Oncology Research 24(5) Abstracts

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Oncology Research, Vol. 24, pp. 287-293, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14648701447779
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of Rap1b Enhances Apoptosis and Autophagy in Gastric Cancer Cells via the PI3K/Akt/mTOR Pathway

Yazhou Li,* Yang Liu,† Feiyu Shi,‡ Liang Cheng,‡ and Junjun She‡

*Department of Interventional Radiology, Hi-Tech People Hospital, BaoJi, China
†Department of General Surgery, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China
‡Department of Orthopaedics, Honghui Hospital, Xi’an Jiaotong University, Xi’an, China

Gastric cancer (GC) is the fourth most common malignancy and the second leading cause of cancer mortality around the world. However, the regulatory mechanisms of GC tumorigenesis and cancer cell motility are completely unknown. We investigated the role of a RAS-related protein (Rap1b) in the progression of GC. Our results showed that the expression of Rap1b is aberrantly upregulated in GC tissue samples and human GC cell lines, and the high expression of Rap1b indicated a positive correlation with poor prognosis in patients with GC. Inhibition of endogenous Rap1b dramatically reduced the cell cycle progression but strongly enhanced the apoptosis capacity of human GC cell lines MKN-28 and SGC-7901 cells compared with the control group. Western blotting assay showed that Rap1b inhibition resulted in a significant increase in the ratio of LC3-II to LC3-I, and the levels of p62 protein were decreased in both MKN-28 and SGC-7901 cells. Furthermore, PI3K/Akt/mTOR activation was found to be maintained in a low level in the normal gastric mucosal epithelial cells, while it was significantly upregulated in GC cells, which could be decreased by Rap1b inhibition. The PI3K inhibitor LY294002 was enhanced but activator insulin-like growth factor 1 (IGF-1) blocked the Rap1b silencing-induced enhancement of apoptosis and autophagy in MKN-28 and SGC-7901 cells. In conclusion, we demonstrate that Rap1b expression is aberrantly increased in GC, resulting in the inhibition of autophagy and apoptosis of GC cells by the PI3K/Akt/mTOR pathway. This might provide a new understanding and represent a novel therapeutic target for human GC.

Key words: Gastric cancer (GC); Rap1b; Autophagy; Apoptosis; PI3K/Akt/mTOR pathway

Address correspondence to Junjun She, Department of General Surgery, First Affiliated Hospital of Xi’an Jiaotong University, Yanta Xi Road No. 277, Xi’an 710061, China. Tel: +86-0917-3532633; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 295-303, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14648701447814
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

Anexelekto (AXL) Increases Resistance to EGFR-TKI and Activation of AKT and ERK1/2 in Non-Small Cell Lung Cancer Cells

Yaqiong Tian,*1 Zengli Zhang,†1 Liyun Miao,* Zhimin Yang,† Jie Yang,* Yinhua Wang,§ Danwen Qian,¶ Hourong Cai,* and Yongsheng Wang*

*Department of Respiratory Medicine, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing, China
†Department of Respiratory Diseases, The Second Affiliated Hospital of Soochow University, Suzhou, China
‡Department of Medical Oncology, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui Province, China
§Department of Oncology, Wuhu No.2 People’s Hospital, Wuhu, Anhui Province, China
¶Department of Oncology, Nanjing Red Cross Hospital, Nanjing, Jiangsu Province, China

Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and overexpressing AXL in PC9 using genetic tools can restore and decrease the sensitivity to gefitinib, respectively. We found that silencing AXL could sensitize the resistance to gefitinib, and the downstream pathways were significantly inhibited. Interestingly, we also discovered that increased AXL expression did promote the resistance, and its downstream targets were activated accordingly. Then 69 NSCLC patients who harbored EGFR mutation were recruited to analyze the expression of AXL and the association between AXL expression and clinical characteristics. We found that 5 of the 69 patients were AXL positive (about 7%), and AXL was related to tumor differentiation and tumor size. In this study, we concluded that the molecular mechanisms of AXL mediated resistance involved in the increased activity of the PI3K/AKT and MAPK/ERK1/2 pathways, and AXL overexpression could promote resistance, but it can be weakened when AXL expression is silenced.

Key words: Anexelekto (AXL); Non-small cell lung cancer (NSCLC); Epidermal growth factor receptor (EGFR); Resistance

1These authors provided equal contribution to this work.
Address correspondence to Yongsheng Wang, Department of Respiratory Medicine, Drum Tower Hospital Affiliated to Medical School of Nanjing University, No. 321 Zhongshan Road, Nanjing, Jiangsu Province 210008, China. Tel: 86-025-83106666; Fax: 86-025-68183333; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 305-313, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14666990347437
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

TIPE2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Prostate Cancer Cells by Inhibiting PI3K/Akt Signaling Pathway

Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, and Yuan-wei Li

Department of Urology, Hunan Provincial People’s Hospital, Changsha, Hunan, China

Tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer cells. Mechanistically, TIPE2 overexpression obviously inhibits the phosphorylation levels of phosphatidylinositol 3-kinase (PI3K) and Akt in prostate cancer cells. In conclusion, for the first time we demonstrated that TIPE2 overexpression may suppress proliferation, migration, and invasion in prostate cancer cells by inhibiting the PI3K/Akt signaling pathway. Therefore, TIPE2 might serve as a potential therapeutic target for human prostate cancer.

Key words: Tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (TNFAIP8L2, TIPE2); Prostate cancer; Epithelial–mesenchymal transition (EMT); PI3K/Akt signaling

Address correspondence to Yuan-wei Li, Department of Urology, Hunan Provincial People’s Hospital, No. 69 of West Jiefang Road, Changsha, Hunan 410008, China. Tel: +86-0731-82278120; Fax: +86-0731-82278012; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 315-325, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14666990347590
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

Liu Feng,*† Wang Wei,* Zhang Heng,† Han Yantao,‡ and Wang Chunbo‡

*Medical College, Qingdao University, Qingdao, China
†Pharmaceutical Department, Qingdao Hiser Medical Center, Qingdao, China
‡Department of Pharmacology, Medical College, Qingdao University, Qingdao, China

REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, knockdown of REV7 can promote TGF-β1 expression. Western blot analysis indicated that TGF-β1 may play a role as a downstream factor of REV7. Moreover, interference of TGF-β1 can also inhibit the cell’s ability for migration, invasion, and EMT, as well as in a cell line whose REV7 is overexpressed. Taken together, these results contributed to a recognition of the oncogene functions of REV7 in breast cancer cells and provided a novel direction to treat breast cancer. 

Key words: REV7; Breast cancer; Epithelial–mesenchymal transition (EMT); Transforming growth factor-β1 (TGF-β1)

Address correspondence to Wang Chunbo, Department of Pharmacology, Medical College, Qingdao University, 308 Ningxia Road, Qingdao

266071, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 327-335, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14666990347635
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

Ritonavir Interacts With Belinostat to Cause Endoplasmic Reticulum Stress and Histone Acetylation in Renal Cancer Cells

Makoto Isono, Akinori Sato, Kazuki Okubo, Takako Asano, and Tomohiko Asano

Department of Urology, National Defense Medical College, Tokorozawa, Saitama, Japan

The histone deacetylase (HDAC) inhibitor belinostat increases the amount of unfolded proteins in cells by promoting the acetylation of heat shock protein 90 (HSP90), thereby disrupting its chaperone function. The human immunodeficiency virus protease inhibitor ritonavir, on the other hand, not only increases unfolded proteins by suppressing HSP90 but also acts as a proteasome inhibitor. We thought that belinostat and ritonavir together would induce endoplasmic reticulum (ER) stress and kill renal cancer cells effectively. The combination of belinostat and ritonavir induced drastic apoptosis and inhibited the growth of renal cancer cells synergistically. Mechanistically, the combination caused ER stress (evidenced by the increased expression of the ER stress markers) and also enhanced histone acetylation by decreasing the expression of HDACs. To our knowledge, this is the first study that showed a beneficial combined effect of belinostat and ritonavir in renal cancer cells, providing a framework for testing the combination in renal cancer patients.

Key words: Belinostat; Ritonavir; Endoplasmic reticulum (ER) stress; Renal cell cancer

Address correspondence to Akinori Sato, Department of Urology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan. Tel: +81-4-2995-1676; Fax: +81-4-2996-5210; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 337-343, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14666990347671
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of Long Noncoding RNA uc.338 by siRNA Inhibits Cellular Migration and Invasion in Human Lung Cancer Cells

Xuexin Gao,* Xuezhen Gao,† Chao Li,* Yukun Zhang,* and Lei Gao‡

*Department of Thoracic Surgery, Central Hospital of Tai’an, Tai’an, Shandong, China
†Operation Room, People’s Hospital of Xin Tai, Xin Tai, Shandong, China
‡Shandong Provincial Research Center for Bioinformatic Engineering and Technique, School of Life Sciences, Shandong University of Technology, Zibo, Shandong, China

Lung cancer remains a critical health concern worldwide. Long noncoding RNAs with ultraconserved elements have recently been implicated in human tumorigenesis. The present study investigated the role of ultraconserved element 338 (uc.338) in the regulation of cell proliferation and metastasis in human lung cancer. Our data showed that the expression of uc.338 in lung cancer was remarkably increased in vivo and in vitro. Depletion of uc.338 with specific siRNA interference retarded the cell proliferative rate in lung cancer cell lines NCI-H929 and H1688. Furthermore, knockdown of uc.338 caused cell cycle arrest in the G0/G1 phase in both cell lines. Transwell assays showed that inhibition of uc.338 notably decreased migration and invasion in NCI-H929 and H1688 cells. Moreover, uc.338 depletion decreased the expression of cyclin B1, Cdc25C, Snail, vimentin, and N-cadherin while increasing the protein level of E-cadherin, shown with Western blot analysis. These results suggested the pro-oncogenic potential of uc.338 in lung cancer, which might provide novel clues for the diagnosis and treatment of lung cancer in the clinic.

Key words: Ultraconserved element 338 (uc.338); Lung cancer; Proliferation; Metastasis; Epithelial–mesenchymal transition (EMT)

Address correspondence to Xuexin Gao, Department of Thoracic Surgery, Central Hospital of Tai’an, No. 29, Long Tan Road, Tai’an, Shandong 271000, China. Tel: +86-0538-8223227; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Lei Gao, Ph.D., Shandong Provincial Research Center for Bioinformatic Engineering and Technique, School of Life Sciences, Shandong University of Technology, No. 266, Xincun West Road, Zhangdian District, Zibo, Shandong 255049, China. Tel: +86-0532-86042052; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 345-351, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14685034103194
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
Printed in the USA. All rights reserved

MicroRNA-16-1 Inhibits Tumor Cell Proliferation and Induces Apoptosis in A549 Non-Small Cell Lung Carcinoma Cells

Weihua Wang,* Jie Chen,* Jinhua Dai,† Burong Zhang,* Feng Wang,* and Yizhe Sun‡

*Department of Clinical Laboratory, The Affiliated Hospital of School of Medicine of Ningbo University, Ningbo, Zhejiang, China
†Department of Clinical Laboratory, Ningbo No. 2 Hospital, Ningbo, Zhejiang, China
‡Wuhan Hospital for the Prevention and Treatment of Occupational Disease, Wuhan, Hubei, China

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Plenty of microRNAs (miRs), except miR-16-1, have been reported to be associated with the initiation and progression of NSCLC. This study was aimed to explore the impacts of miR-16-1 on NSCLC cells. Human NSCLC cell line A549 was used, and the expression of miR-16-1 was up- or downregulated by transfecting with miR-16-1 mimics or inhibitors. Afterward, cell proliferation and apoptosis were detected using MTT assay, BrdU assay, and Annexin V/FITC Apoptosis Detection Kit. The expression changes of proliferation- and apoptosis-related factors were measured by Western blot. Results showed that miR-16-1 overexpression significantly inhibited cell proliferation and induced apoptosis when compared with the control group. Besides, miR-16-1 overexpression significantly upregulated the protein expressions of p27, Bax, procaspase 3, and cleaved caspase 3, whereas it downregulated Bcl-2. Conversely, miR-16-1 suppression affected NSCLC cell proliferation and apoptosis, and these protein expressions resulted in completely opposite impacts. In conclusion, miR-16-1 overexpression could inhibit cell proliferation and induce apoptosis via regulating the expression of p27, Bcl-2, Bax, and caspase 3 in NSCLC cells.

Key words: MicroRNA-16-1; Non-small cell lung cancer (NSCLC); Cell proliferation; Apoptosis

Address correspondence to Yizhe Sun, Wuhan Hospital for the Prevention and Treatment of Occupational Disease, No. 18 Jianghan North Road, Wuhan 430015, Hubei, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 353-360, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14685034103275
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
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Suppressive Role of MicroRNA-148a in Cell Proliferation and Invasion in Ovarian Cancer Through Targeting Transforming Growth Factor-β-Induced 2

Min Zhao,* Zhiying Su,† Shiyang Zhang,‡ Liangjin Zhuang,§ Yudi Xie,* and Xiaodong Li*

*Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China
†Department of Obstetrics, Maternal and Child Health Hospital of Xiamen City, Xiamen, Fujian, China
‡Department of Hospital Infection-Control, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China
§Early cancer screening center, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China

Ovarian cancer (OC) is one of the most common gynecological malignancies. MicroRNAs (miRs) play a crucial role in the development and progression of OC, but the underlying mechanism remains largely unclear. Our study investigated the regulatory role of miR-148a in OC cell proliferation and invasion. We found that miR-148a was significantly downregulated in OC tissues compared to their matched adjacent nontumor tissues. In addition, its expression was also reduced in OC cell lines (SKOV3, ES-2, OVCAR, and A2780) compared to normal ovarian epithelial cells. Overexpression of miR-148a caused a significant decrease in OC cell proliferation and invasion, as well as reduced MMP9 protein levels. Transforming growth factor-β-induced 2 (TGFI2) was further identified as a target gene of miR-148a, and its protein expression was downregulated in OC cells after miR-148a overexpression. Restoration of TGFI2 attenuated the suppressive effects of miR-148a on OC cell proliferation and invasion. Moreover, we found that TGFI2 was remarkably upregulated in OC tissues when compared with their matched adjacent nontumortissues, and observed a reverse correlation between miR-148a and TGFI2 expression in OC tissues. On the basis of these findings, we suggest that miR-148a inhibits OC cell proliferation and invasion partly through inhibition of TGFI2. Therefore, our study highlights the importance of the miR-148a/TGFI2 axis in the malignant progression of OC.

Key words: Ovarian cancer (OC); MicroRNAs (miRs); Transforming growth factor-β-induced 2 (TGFI2); Proliferation; Invasion

Address corresponding to Min Zhao, Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Xiamen University, 55 Zhenhai Road, Xiamen, Fujian, China. Tel: +86-592-2137292; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 361-369, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14685034103310
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
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Knockdown of UBE2T Inhibits Osteosarcoma Cell Proliferation, Migration, and Invasion by Suppressing the PI3K/Akt Signaling Pathway

Yu Wang,*†1 Hui Leng,†1 Hui Chen,*‡ Lei Wang,* Nan Jiang,* Xin Huo,† and Bin Yu*

*Department of Orthopaedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou, P.R. China
†Department of Orthopaedics, Chifeng Hospital, Inner Mongolia, P.R. China
‡Department of Pediatric Orthopaedics, the Second Hospital of Fuzhou Affiliated to Xiamen University, Fuzhou, P.R. China

Ubiquitin-conjugating enzyme E2T (UBE2T), a member of the E2 family, was found to be overexpressed in a great many cancers such as bladder cancer, lung cancer, and prostate cancer. However, there have been no reports on the role of UBE2T in osteosarcoma. In this study, we tried to make the effects of UBE2T on osteosarcoma clear. The study results showed that UBE2T was overexpressed in osteosarcoma tissues and cell lines. Moreover, UBE2T knockdown inhibited osteosarcoma cell proliferation, migration, and invasion. We also observed that UBE2T downregulation could suppress the activity of the PI3K/Akt signaling pathway. Therefore, we concluded that UBE2T exerted its inhibitory effects on osteosarcoma cells via suppressing the PI3K/Akt signaling pathway. These findings indicated that UBE2T may be a potential therapeutic target for osteosarcoma treatment.

Key words: Ubiquitin-conjugating enzyme E2T (UBE2T); Osteosarcoma; Proliferation; Invasion; PI3K/Akt signaling pathway

1These authors provided equal contribution to this work.
Address correspondence to Bin Yu, Department of Orthopaedics and Traumatology, Nanfang Hospital, Southern Medical University, No. 1838, North of Guangzhou Avenue, Guangzhou 510515, P.R. China. Tel: +86-020-61641741; Fax: +86-020-61641741; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 371-380, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14685034103356
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
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MicroRNA-21 Regulates the Proliferation, Differentiation, and Apoptosis of Human Renal Cell Carcinoma Cells by the mTOR-STAT3 Signaling Pathway

Tao Liang, Xiao-Yong Hu, Yong-Hui Li, Bin-Qiang Tian, Zuo-Wei Li, and Qiang Fu

Department of Urology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, P.R. China

MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value of cells, inhibited mRNA expression of PPARγ and C/EBPα, and enhanced activity of caspase 3. Furthermore, protein expression of pSTAT3 was also decreased in the absence of miRNA-21. Notably, miRNA-21-changed proliferation, differentiation, and apoptosis of human RCC cells were partially regulated following the block of the mTOR-STAT3 signaling pathway by the mTOR inhibitor (XL388). It was indicated that miRNA-21 promoted proliferation and differentiation and decreased apoptosis of human RCC cells through the activation of the mTOR-STAT3 signaling pathway.

Key words: miRNA-21; Human renal cell carcinoma (RCC); Proliferation; Differentiation; Apoptosis; mTOR; STAT3

Address correspondence to Tao Liang, Department of Urology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, No. 600 Yi Shan Road, Shanghai 200233, P.R. China. Tel: +862138297582; Fax: +862138297582; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 381-389, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14685034103392
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC.
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Armadillo Repeat-Containing Protein 8 (ARMC8) Silencing Inhibits Proliferation and Invasion in Osteosarcoma Cells

Feng Jiang,*1 Yan Shi,†1 Hong Lu,† and Guojun Li*

*Department of Orthopedics, Huaihe Hospital of Henan University, Kaifeng, Henan Province, P.R. China
†Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, Henan Province, P.R. China

Armadillo repeat-containing protein 8 (ARMC8) plays an important role in regulating cell migration, proliferation, tissue maintenance, signal transduction, and tumorigenesis. However, the expression pattern and role of ARMC8 in osteosarcoma are still unclear. In this study, our aims were to examine the effects of ARMC8 on osteosarcoma and to explore its underlying mechanism. Our results demonstrated that ARMC8 was overexpressed in osteosarcoma cell lines. Knockdown of ARMC8 significantly inhibited osteosarcoma cell proliferation in vitro and markedly inhibited xenograft tumor growth in vivo. ARMC8 silencing also suppressed the epithelial–mesenchymal transition (EMT) phenotype, as well as inhibited the migration and invasion of osteosarcoma cells. Furthermore, knockdown of ARMC8 obviously inhibited the expression of β-catenin, c-Myc, and cyclin D1 in MG-63 cells. In conclusion, this report demonstrates that ARMC8 silencing inhibits proliferation and invasion of osteosarcoma cells. Therefore, ARMC8 may play an important role in the development and progression of human osteosarcoma and may represent a novel therapeutic target in the treatment of osteosarcoma.

Key words: Armadillo repeat-containing protein 8 (ARMC8); Osteosarcoma; Proliferation; Invasion

1These authors provided equal contribution to this work.
Address correspondence to Yan Shi, Department of Oncology, Huaihe Hospital of Henan University, No. 8 Baobei Road, Kaifeng 475000, Henan Province, P.R. China. Tel: +86-0371-23906644; Fax: +86-0371-23906644; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it