Oncology Research 27(3) Abstracts

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Oncology Research, Vol. 27, pp. 283-292, 2019
0965-0407/19 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15035795904677
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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G-Protein-Coupled Estrogen Receptor Antagonist G15 Decreases Estrogen-Induced Development of Non-Small Cell Lung Cancer

Changyu Liu,* Yongde Liao,* Sheng Fan,* Xiangning Fu,* Jing Xiong,† Sheng Zhou,† Man Zou,‡ and Jianmiao Wang§

*Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, P.R. China
†Department of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, P.R. China
‡Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, P.R. China
§Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, P.R. China

G-protein-coupled estrogen receptor (GPER) was found to promote non-small cell lung cancer (NSCLC) by estrogen, indicating the potential necessity of inhibiting GPER by a selective antagonist. This study was performed to elucidate the function of GPER-selective inhibitor G15 in NSCLC development. Cytoplasmic GPER (cGPER) and nuclear GPER (nGPER) were detected by immunohistochemical analysis in NSCLC samples. The relation of GPER and estrogen receptor
β (ERβ) expression and correlation between GPER, ERβ, and clinical factors were analyzed. The effects of activating GPER and function of G15 were analyzed in the proliferation of A549 and H1793 cell lines and development of urethane-induced adenocarcinoma. Overexpression of cGPERand nGPER was detected in 80.49% (120/150) and 52.00% (78/150) of the NSCLC samples. High expression of GPER was related with higher stages, poorer differentiation, and high expression of ERβ. The protein level of GPER in the A549 and H1793 cell lines was increased by treatment with E2, G1 (GPER agonist), or fulvestrant (Ful; ERβ antagonist) and decreased by G15. Administration with G15 reversed the E2- or G1-induced cell growth by inhibiting GPER. In urethane-induced adenocarcinoma mice, the number of tumor nodules and tumor index increased in the E2 or G1 group and decreased by treatment with G15. These findings demonstrate that using G15 to block GPER signaling may be considered as a new therapeutic target in NSCLC.

Key words: G15; G-protein-coupled estrogen receptor (GPER); Non-small cell lung cancer (NSCLC); G1; E2

Address correspondence to Yongde Liao, Department of Thoracic Surgery, Tongji Hospital, 1095 Jiefang Dadao Street, Wuhan, Hubei Province 430030, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 293-299, 2019
0965-0407/19 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15190399381143
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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miR-615 Inhibits Prostate Cancer Cell Proliferation and Invasion by Directly Targeting Cyclin D2

Fengyu Huang,*† Hongjun Zhao,† Zhaojin Du,‡ and Hong Jiang§

*Qingdao University, Qingdao, P.R. China
†Department of Urology, Yantai Municipal Laiyang Central Hospital, Laiyang, Shandong Province, P.R. China
‡Reproductive Medical Center, Qingdao Women and Children’s Hospital, Qingdao University, Qingdao, Shandong Province, P.R. China
§Department of Gastroenterology, Yantai Municipal Laiyang Central Hospital, Laiyang, Shandong Province, P.R. China

Previous studies have reported that miR-615 exerts a tumor suppressor role in some tumors, such as esophageal squamous cell carcinoma and non-small cell lung cancer. However, the role of miR-615 in prostate cancer has not been defined. Here we found that miR-615 was downregulated in prostate cancer tissues and cell lines. Overexpression of miR-615 in PC-3 cells significantly inhibited cellular proliferation, migration, and invasion. Moreover, overexpression of miR-615 delayed tumor growth in vivo. In terms of mechanism, we found that cyclin D2 (CCND2) is a target gene of miR-615 in prostate cancer. We showed that miR-615 could bind to the 3
-UTR region of CCND2 mRNA and inhibit its expression. There was a negative correlation between the expression of miR-615 and CCND2 in prostate cancer tissues. Moreover, restoration of cyclin D2 abolished the inhibitory effects of miR-615 on the proliferation, migration, and invasion of prostate cancer cells. Taken together, our study identified miR-615 as a tumor suppressor by targeting cyclin D2 in prostate cancer.

Key words: miR-615; Prostate cancer; Proliferation; Migration; Cyclin D2

Address correspondence to Hong Jiang, Department of Gastroenterology, Yantai Municipal Laiyang Central Hospital, No. 111 Changshan Road, Laiyang 265200, Shandong Province, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 301-309, 2019
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DOI: https://doi.org/10.3727/096504018X
15213058045841
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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MicroRNA-1277 Inhibits Proliferation and Migration of Hepatocellular Carcinoma HepG2 Cells by Targeting and Suppressing BMP4 Expression and Reflects the Significant Indicative Role in Hepatocellular Carcinoma Pathology and Diagnosis After Magnetic Resonance Imaging Assessment

Xinshan Cao,* Ling Xu,† Quanyuan Liu,* Lijuan Yang,‡ Na Li,§ and Xiaoxiao Li*

*Department of Radiology, Binzhou Medical University Hospital, Binzhou, Shandong, P.R. China
†Department of Liver Disease Center, Traditional Chinese Medicine Hospital of Binzhou City, Binzhou, Shandong, P.R. China
‡Department of Experiment Center of Tumor, Binzhou Medical University Hospital, Binzhou, Shandong, P.R. China
§Department of Clinical Laboratory, Binzhou Medical University Hospital, Binzhou, Shandong, P.R. China

Our study aimed to investigate the roles and possible regulatory mechanism of miR-1277 in the development of hepatocellular carcinoma (HCC). HCC patients were identified from patients who were diagnosed with focal liver lesions using magnetic resonance imaging (MRI). The expression levels of miR-1277 in the serum of HCC patients and HepG2 cells were measured. Then miR-1277 mimic, miR-1277 inhibitor, or scramble RNA was transfected into HepG2 cells. The effects of miR-1277 overexpression and suppression on HepG2 cell proliferation, migration, and invasion were then investigated. Additionally, the expression levels of epithelial–mesenchymal transition (EMT)-related markers, including E-cadherin,
β-catenin, and vimentin, were detected. Target prediction and luciferase reporter assay were performed to explore the potential target of miR-1277. miR-1277 was significantly downregulated in the serum of HCC patients and HepG2 cells. Suppression of miR-1277 promoted HepG2 cell proliferation, migration, and invasion, whereas overexpression of miR-1277 had opposite effects. In addition, after miR-1277 was suppressed, the expressions of E-cadherin and β-catenin were significantly increased, while the expressions of vimentin were markedly decreased. Bone morphogenetic protein 4 (BMP4) was identified as the direct target of miR-1277. Knockdown of BMP4 reversed the effects of miR-1277 suppression on HepG2 cell migration and invasion, as well as the expressions of E-cadherin, β-catenin, and vimentin. Our results indicate that downregulation of miR-1277 may promote the migration and invasion of HepG2 cells by targeting BMP4 to induce EMT. Combination of MRI and miR-1277 level will facilitate the diagnosis and treatment of HCC.

Key words: Hepatocellular carcinoma (HCC); Bone morphogenetic protein 4 (BMP4); miR-1277; Magnetic resonance imaging (MRI)

Address correspondence to Xinshan Cao, Department of Radiology, Binzhou Medical University Hospital, No. 661 Huanghe Second Road, Binzhou, Shandong 256603, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 311-316, 2019
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DOI: https://doi.org/10.3727/096504018X
15220579006875
E-ISSN 1555-3906
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miR-455 Functions as a Tumor Suppressor Through Targeting GATA6 in Colorectal Cancer

Hua Yunqi,*1 Yin Fangrui,†1 Yang Yongyan,* Jin Yunjian,* Zhang Wenhui,* Cao Kun,* Li Min,* Liu Xianfeng,* and Ba Caixia*

*Cancer Biotherapy Center and Oncology Department, Baotou Tumor Hospital, Clinical Oncology of Baotou Medical College, Baotou, Inner Mongolia, P.R. China
†Department of Central Laboratory, The First Affiliated Hospital of Baotou Medical College, Baotou, Inner Mongolia, P.R. China

Emerging evidence indicates that microRNAs (miRNAs) are often aberrantly expressed in human cancers. Meanwhile, the importance of miRNAs in regulating multiple cellular biological processes has been appreciated. The aim of this study was to investigate the significance of miR-455 and identify its possible mechanism in regulating colorectal cancer (CRC) progression. We found that the expression of miR-455 was sharply reduced in CRC tissues and cell lines. Importantly, the low expression of miR-455 was associated with poor overall survival of CRC patients. Overexpression of miR-455 in CRC cell lines significantly inhibited cell proliferation and migration in vitro. Moreover, GATA-binding protein 6 (GATA6), whose expression can be inversely regulated by miR-455 in CRC cell lines, was validated as a direct target of miR-455. Overall, our results revealed that miR-455 functions as a tumor suppressor, and its downregulation may contribute to CRC progression. Our study may provide a novel therapeutic target for CRC in the future.

Key words: miR-455; Colorectal cancer (CRC); GATA6; Proliferation; Migration

1These authors provided equal contribution to this work.
Address correspondence to Liu Xianfeng, Cancer Biotherapy Center and Oncology Department, Baotou Tumor Hospital, Clinical Oncology of Baotou Medical College, No. 18 United Street, Qingshan District, Baotou, Inner Mongolia 014030, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Ba Caixia, Cancer Biotherapy Center and Oncology Department, Baotou Tumor Hospital, Clinical Oncology of Baotou Medical College, No. 18 United Street, Qingshan District, Baotou, Inner Mongolia 014030, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 317-323, 2019
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DOI: https://doi.org/10.3727/096504018X
15228863026239
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

Xiyan Sun,*1 Chao Zhang,†1 Yang Cao,† and Erbiao Liu*

*Department of Oncology, Shanxian Central Hospital, Heze, Shandong Province, P.R. China
†Department of Dermatology, Shanxian Central Hospital, Heze, Shandong Province, P.R. China

miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there was an inverse correlation between the expression of miR-150 and MYB in melanoma tissues. We also showed that MYB was upregulated in melanoma tissues and cell lines. Through functional experiments, we found that restoration of MYB in miR-150-overexpressed melanoma cells rescued the proliferation, migration, and invasion. Therefore, our findings demonstrated that miR-150 suppressed the proliferation, migration, and invasion of melanoma cell by downregulating MYB.

Key words: miR-150; MYB; Proliferation; Invasion; Melanoma

1These authors provided equal contribution to this work and are co-first authors.
Address correspondence to Erbiao Liu, Department of Oncology, Shanxian Central Hospital, No. 1 Cultural Road, Heze 274300, Shandong Province, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 325-334, 2019
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DOI: https://doi.org/10.3727/096504018X
15251282086836
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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Overexpression of miR-1283 Inhibits Cell Proliferation and Invasion of Glioma Cells by Targeting ATF4

Hao Chen, Yi Zhang, Hai Su, Hui Shi, Qijiang Xiong, and Zulu Su

Department of Neurosurgery, Yongchuan Hospital of Chongqing Medical University, Chongqing, P.R. China

It is well known that activating transcription factor 4 (ATF4) expression is closely associated with progression of many cancers. We found that miR-1283 could directly target ATF4. However, the precise mechanisms of miR-1283 in glioma have not been well clarified. Our study aimed to explore the interaction between ATF4 and miR-1283 in glioma. In this study, we found that the level of miR-1283 was dramatically decreased in glioma tissues and cell lines, the expression of ATF4 was significantly increased, and the low level of miR-1283 was closely associated with high expression of ATF4 in glioma tissues. Moreover, introduction of miR-1283 significantly inhibited proliferation and invasion of glioma cells. However, knockdown of miR-1283 promoted the proliferation and invasion in glioma cells. Bioinformatics analysis predicted that the ATF4 was a potential target gene of miR-1283. Luciferase reporter assay demonstrated that miR-1283 could directly target ATF4. In addition, knockdown of ATF4 had similar effects with miR-1283 overexpression on glioma cells. Upregulation of ATF4 in glioma cells partially reversed the inhibitory effects of miR-1283 mimic. Overexpression of miR-1283 inhibited cell proliferation and invasion of glioma cells by directly downregulating ATF4 expression.

Key words: Glioma; MicroRNA-1283; Activating transcription factor 4 (ATF4); Proliferation; Invasion

Address correspondence to Zulu Su, Department of Neurosurgery, Yongchuan Hospital of Chongqing Medical University, No. 439 Xuanhua Road, Yongchuan District, Chongqing 402160, P.R. China. Tel: +86-023-85382926; Fax: +86-023-85382926; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 335-340, 2019
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DOI: https://doi.org/10.3727/096504018X
15252202178408
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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MicroRNA-152 Acts as a Tumor Suppressor MicroRNA by Inhibiting Krüppel-Like Factor 5 in Human Cervical Cancer

Haiyan Zhang,*† Yanxia Lu,‡ Surong Wang,‡ Xiugui Sheng,§ and Shiqian Zhang*

*Department of Gynecology, Affiliated Qilu Hospital of Shandong University, Lixia District, Jinan, Shandong, P.R. China
†Department of Gynecology Ward-1, Linyi People’s Hospital, Hedong District, Linyi, Shandong, P.R. China
‡Department of Gynecology Ward-3, Linyi People’s Hospital, Linyi, Hedong District, Linyi, Shandong, P.R. China
§Department of Gynecology, Cancer Hospital Chinese Academy of Medical Sciences, Chaoyang District, Beijing, P.R. China

Aberrant expression of microRNA-152 (miR-152) is frequently observed in human cancers including ovarian cancer, breast cancer, prostate cancer, and gastric cancer. However, its expression and functional role in cervical cancer (CC) are poorly understood. Also, the association between miR-152 and Krüppel-like factor 5 (KLF5) expression in CC remains unclear. In this study, analyzing the expression of miR-152 by quantitative real-time PCR (qRT-PCR) revealed it was sharply reduced in CC tissues and cell lines. In addition, the negative correlation of miR-152 expression and KLF5 expression was observed. The dual-luciferase reporter assay validated that KLF5 was a target of miR-152. In vitro functional assays revealed that miR-152 could inhibit cell proliferation and cell cycle progression through regulating the expression of KLF5. Taken together, our study suggested that miR-152 functions as a tumor suppressor in CC, and the miR-152/KLF5 axis may provide novel therapeutic targets for CC treatment.

Key words: miR-152; Cervical cancer (CC); Krüppel-like factor 5 (KLF5); Proliferation; Cell cycle

Address correspondence to Shiqian Zhang, Department of Gynecology, Affiliated Qilu Hospital of Shandong University, No. 127 West Cultural Road, Lixia District, Jinan, Shandong 250012, P.R. China. Tel: +86 0531-82169114; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 341-347, 2019
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DOI: https://doi.org/10.3727/096504018X
15228909735079
E-ISSN 1555-3906
Copyright ©2019 Cognizant, LLC.
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lncRNA MNX1-AS1 Promotes Glioblastoma Progression Through Inhibition of miR-4443

Yan Gao, Yongchuan Xu, Jue Wang, Xue Yang, Lulu Wen, and Juan Feng

Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University, Shenyang, P.R. China

Long noncoding RNAs (lncRNAs) have been acknowledged as important regulators in various human cancers. lncRNA MNX1-AS1 has been shown to be an oncogene in epithelial ovarian cancer. However, the function of MNX1-AS1 in glioblastoma (GBM) remains largely unknown. Here we found that the expression of MNX1-AS1 was significantly upregulated in GBM tissues and cell lines. Knockdown of MNX1-AS1 significantly inhibited the proliferation, migration, and invasion of GBM cells. In terms of mechanism, we found that MNX1-AS1 could bind to miR-4443 in GBM cells. Overexpression of miR-4443 significantly inhibited the expression of MNX1-AS1 and vice versa. Moreover, there was an inverse correlation between the expression levels of MNX1-AS1 and miR-4443 in GBM tissues. We found that overexpression of miR-4443 inhibited the proliferation, migration, and invasion of GBM cells. We also showed that inhibition of miR-4443 reversed the effects of MNX1-AS1 knockdown on GBM cell proliferation, migration, and invasion. Taken together, we found that MNX1-AS1 promoted the proliferation, migration, and invasion of GBM cells through inhibiting miR-4443.

Key words: MNX1-AS1; Proliferation; Migration; miR-4443; Glioblastoma (GBM)

Address correspondence to Juan Feng, Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang 110004, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 349-358, 2019
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DOI: https://doi.org/10.3727/096504018X
15247361080118
E-ISSN 1555-3906
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MicroRNA-411 Inhibits Cervical Cancer Progression by Directly Targeting STAT3

Dan Shan, Yumin Shang, and Tongxiu Hu

Department of Obstetrics and Gynecology, Tianjin Hospital, Tianjin, P.R. China

Cervical cancer is the third most common gynecological cancer and the fourth leading cause of cancer-related deaths in women around the world. Substantial evidence has demonstrated that microRNA (miRNA) expression is disordered in many malignant tumors. The dysregulation of miRNAs has been suggested to be involved in the tumorigenesis and tumor development of cervical cancer. Therefore, identification of miRNAs and their biological roles and targets involved in tumor pathology would provide valuable insight into the diagnosis and treatment of patients with cervical cancer. MicroRNA-411 (miR-411) has been reported to play an important role in several types of human cancer. However, the expression level, role, and underlying molecular mechanisms of miR-411 in cervical cancer remain unclear. Therefore, the objectives of this study were to investigate the expression pattern and clinical significance of miR-411 in cervical cancer and to evaluate its role and underlying mechanisms in this disease. In this study, we confirmed that the expression of miR-411 was significantly downregulated in both cervical cancer tissues and cell lines. Low expression of miR-411 was associated with tumor size, FIGO stage, lymph node metastasis, and distant metastasis. Additionally, miR-411 overexpression inhibited cell proliferation and invasion in cervical cancer. Furthermore, signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-411 in this disease. In clinical samples, miR-411 expression levels were inversely correlated with STAT3, which was significantly upregulated in cervical cancer. Restored STAT3 expression abolished the tumor-suppressing effects of miR-411 overexpression on the proliferation and invasion of cervical cancer cells. In conclusion, our data demonstrated that miR-411 inhibited cervical cancer progression by directly targeting STAT3 and may represent a novel potential therapeutic target and prognostic marker for patients with this disease.

Key words: Cervical cancer; MicroRNA-411; Proliferation; Invasion; Signal transducer and activator of transcription 3 (STAT3)

Address correspondence to Tongxiu Hu, Department of Obstetrics and Gynecology, Tianjin Hospital, No. 406 Jiefang South Road, Tianjin 300211, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 359-369, 2019
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DOI: https://doi.org/10.3727/096504018X
15220594629967
E-ISSN 1555-3906
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lncRNA BCAR4 Increases Viability, Invasion, and Migration of Non-Small Cell Lung Cancer Cells by Targeting Glioma-Associated Oncogene 2 (GLI2)

Hongliang Yang,*1 Lei Yan,†1 Kai Sun,‡ Xiaodong Sun,† Xudong Zhang,§ Kerui Cai,† and Tiejun Song*

*Department of Clinical Laboratory, The Second Affiliated Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China
†Department of Histology and Embryology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China
‡Department of Biology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China
§Department of Physiology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, P.R. China

This study aimed to explore the effects of lncRNA BCAR4 on the viability and aggressiveness of non-small cell lung cancer (NSCLC) cells. qRT-PCR was used to determine the expression of BCAR4 and
GLI2 downstream genes in NSCLC tissues and cell lines. Chromatin isolation by RNA purification (CHIRP) and Western blot were employed to measure the expression of the GLI2 downstream proteins. Ki-67 expression in nude mice tumors was tested by immunohistochemistry. MTT assay, wound healing assay, and Transwell assay were used to assess NSCLC cell viability and aggressiveness, respectively. Tumor xenograft was conducted to determine the effects of BCAR4 and GLI2 on NSCLC tumorigenesis in vivo. The expression of BCAR4 in NSCLC tissues and cells was significantly higher than the normal level. The overexpression of BCAR4 promoted NSCLC cell viability, migration, and invasion. The suppression of BCAR4 and GLI2 showed the opposite effects. The overexpression of BCAR4 led to an increase in the expression of GLI2 downstream proteins, while the suppression of BCAR4 and GLI2 reduced their expression. In a tumor xenograft assay, the tumors in mice of the BCAR4 group showed the biggest volume, while those in mice of the si-GLI2 group showed the smallest volume. Ki-67 showed much higher levels in the BCAR4 overexpression group but much lower levels in the si-GLI2 group. In summary, the cooperative mechanism of lncRNA BCAR4 and GLI2 might provide a new opportunity for treating NSCLC.

Key words: GLI2; Long noncoding RNA BCAR4; Non-small cell lung cancer (NSCLC)

1These authors provided equal contribution to this work.
Address correspondence to Tiejun Song, Department of Clinical Laboratory, The Second Affiliated Hospital of Mudanjiang Medical University, No. 15 Dongxiaoyun Street, Aimin District, Mudanjiang 157011, Heilongjiang, P.R. China. Tel.: +86 0453-85939390; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 371-377, 2019
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DOI: https://doi.org/10.3727/096504018X
15178740729367
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Upregulated lncRNA CASC2 May Inhibit Malignant Melanoma Development Through Regulating miR-18a-5p/RUNX1

Yankun Zhang,* Wei Qian,* Feng Feng,† Qian Cao,* Yanqi Li,* Ying Hou,* Luyang Zhang,* and Jufeng Fan*

*Department of Plastic and Reconstructive Surgery, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, P.R. China
†Department of Operating Room, Sanfine International Hospital, Beijing, P.R. China

This study aimed to investigate the effect and underlying mechanism of lncRNA CASC2 in malignant melanoma (MM). Expression of CASC2 in MM tissues and cells was detected. A375 cells were transfected with pc-CASC2, si-CASC2, miR-18a-5p inhibitor, or corresponding controls, and then cell proliferation, migration, and invasion were detected using MTT assay, colony formation assay, and Transwell analysis, respectively. The relationship of miR-18a-5p and CASC2 or RUNX1 was detected by luciferase reporter assay. The levels of CASC2 and RUNX1 were significantly reduced in MM tissues compared with normal skin tissues or cells, while the miR-18a-5p level was obviously increased (all
p < 0.01). Cell viability, colony number, migration, and invasion were significantly decreased in cells with pc-CASC2 compared with cells transfected with pcDNA3.1 (all p < 0.05). These effects were consistent with the cells transfected with miR-18a-5p inhibitor. The luciferase reporter assay revealed that CASC2 acted as a molecular sponge for miR-18a-5p, and RUNX1 was a target gene of miR-18a-5p. Moreover, CASC2 overexpression promoted the expression of RUNX1, while upregulated miR-18a-5p significantly reversed the effect of CASC2 on the RUNX1 level (all p < 0.05). Upregulated CASC2 may inhibit cell proliferation, migration, and invasion through regulating miR-18a-5p and its target gene RUNX1 in MM.

Key words: Malignant melanoma; lncRNA CASC2; miR-18a-5p; Cell proliferation; Migration and invasion

Address correspondence to Jufeng Fan, Department of Plastic and Reconstructive Surgery, Beijing Chao-Yang Hospital, Capital Medical University, No. 8 Workers Stadium South Road, Beijing 100020, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 379-387, 2019
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DOI: https://doi.org/10.3727/096504018X
15199531937158
E-ISSN 1555-3906
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Upregulation of lncRNA CASC2 Suppresses Cell Proliferation and Metastasis of Breast Cancer via Inactivation of the TGF-β Signaling Pathway

Yang Zhang,*† Min Zhu,‡ Yuanbo Sun,§ Wenyuan Li,*† Ying Wang,*† and Weiguang Yu¶

*Research Institute of Neural Tissue Engineering, Mudanjiang College of Medicine, Mudanjiang, P.R. China
†Department of Anatomy, Mudanjiang College of Medicine, Mudanjiang, P.R. China
‡Department of Imaging, Hongqi Hospital, Mudanjiang College of Medicine, Mudanjiang, P.R. China
§Department of Nephrology, Hongqi Hospital, Mudanjiang College of Medicine, Mudanjiang, P.R. China
¶The First Department of General Surgery, Hongqi Hospital, Mudanjiang College of Medicine, Mudanjiang, P.R. China

Breast cancer is one of the major malignancies with a mounting mortality rate in the world. Long noncoding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) has been identified to regulate the initiation and progression of multiple tumorous diseases according to previous studies. However, its biological role has been rarely reported in breast cancer. In the present study, lncRNA CASC2 was found to be significantly downregulated in breast cancer tissues and cell lines using real-time quantitative PCR. Furthermore, gain-of-function assays demonstrated that overexpression of lncRNA CASC2 significantly repressed breast cancer cell proliferation and metastasis. Moreover, CASC2 induced cell cycle arrest and much more early apoptosis of breast cancer. Additionally, based on the above research, we illustrated that inactivation of the TGF-
β signaling pathway was involved in the function of lncRNA CASC2. Collectively, lncRNA CASC2 was a key factor in the tumorigenesis and malignancy of breast cancer, suggesting it may possibly be a potential therapy target for the treatment of breast cancer.

Key words: Long noncoding RNAs (lncRNAs); CASC2; Breast cancer; Transforming growth factor-β (TGF-β)

Address correspondence to Weiguang Yu, The First Department of General Surgery, Hongqi Hospital, Mudanjiang College of Medicine, No. 5 Tongxiang Road, Aimin District, Mudanjiang City 157011, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 389-397, 2019
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DOI: https://doi.org/10.3727/096504018X
15223159811838
E-ISSN 1555-3906
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MicroRNA 495 Inhibits Proliferation and Metastasis and Promotes Apoptosis by Targeting Twist1 in Gastric Cancer Cells

Chao Liu,*† Min Jian,‡ Hong Qi,† and Wei-Zheng Mao†

*Qingdao University, Qingdao, P.R. China
†Department of General Surgery, Qingdao Municipal Hospital, Qingdao, P.R. China
‡Department of Laboratory Medicine, Qingdao Women and Children’s Hospital, Qingdao, P.R. China

Recently, microRNAs (miRNAs) have been reported to participate in multiple biological processes. However, the effects of miR-495 on gastric cancer (GC) remain unclear. The purpose of this study was to explore the functions of miR-495 in GC cell proliferation, metastasis, and apoptosis. SGC-7901 and BGC-823 cell lines were transfected with miR-495 mimic, miR-495 inhibitor, and negative controls (mimic control and inhibitor control). The expressions of miR-495, cell viability, migration, apoptosis, and apoptosis-related factors were examined by qRT-PCR, trypan blue staining, Transwell, flow cytometry, and Western blot, respectively. Simultaneously, key factor expression levels of EMT were detected by qRT-PCR and Western blot. The direct target of miR-495 was confirmed by dual-luciferase assay. Additionally, sh-Twist1, pc-Twist1, and corresponding controls were transfected into SGC-7901 and BGC-823 cells, and the protein levels of EMT-associated factors were detected by Western blot. miR-495was downregulated in GC cells. miR-495 expression level was effectively overexpressed or suppressed in SGC-7901 and BGC-823 cells. Overexpression of miR-495 significantly decreased cell viability and migration, increased apoptosis, and inhibited the EMT process. Suppression of miR-495 showed contrary results. Twist1 was clarified as a target gene of miR-495, and Twist1 silencing obviously reduced the promoting effect of miR-495 suppression on these biological processes. Twist1 silencing significantly blocked the EMT process in both SGC-7901 and BGC-823 cells. miR-495 inhibited proliferation and metastasis and promoted apoptosis by targeting Twist1 in GC cells. These data indicated that miR-495 might be a novel antitumor factor of GC and provide a new method for the treatment of GC.

Key words: Gastric cancer (GC); MicroRNA-495; Proliferation; Apoptosis; Epithelial–mesenchymal transition (EMT); Twist1

Address correspondence to Wei-Zheng Mao, Department of General Surgery, Qingdao Municipal Hospital, No. 5 Donghai Middle Road, Qingdao 266071, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it