Oncology Research 24(3) Abstracts

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Oncology Research, Vol. 24, pp. 137-144, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14611963142218
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of PFTAIRE Protein Kinase 1 (PFTK1) Inhibits Proliferation, Invasion, and EMT in Colon Cancer Cells

Jiankang Zhu, Chongzhong Liu, Fengyue Liu, Yadong Wang, and Min Zhu

Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, China

PFTK1 is a member of the cyclin-dependent kinase (CDK) family and is upregulated in many types of tumors. However, its expression and role in colon cancer remain unclear. In this study, we aimed to investigate the expression and function of PFTK1 in colon cancer. Our results showed that PFTK1 was highly expressed in colon cancer cell lines. The in vitro experiments demonstrated that knockdown of PFTK1 inhibited the proliferation, migration, and invasion of colon cancer cells as well as the epithelial-to-mesenchymal transition (EMT) progress. Furthermore, knockdown of PFTK1 suppressed the expression of Shh as well as Smo, Ptc, and Gli-1 in colon cancer cells. Taken together, these results suggest that knockdown of PFTK1 inhibited the proliferation and invasion of colon cancer cells as well as the EMT progress by suppressing the Sonic hedgehog signaling pathway. Therefore, these findings reveal that PFTK1 may be a potential therapeutic target for the treatment of colon cancer.

Key words: PFTK1; Colon cancer; Invasion; Epithelial-to-mesenchymal transition (EMT)

Address correspondence to Min Zhu, Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, No. 107, Wenhua Xi Road, Jinan 250012, China. Tel: +86-053182166695; Fax: +86-053182166695; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 145-151, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14611963142290
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

MicroRNA-15a Inhibits Proliferation and Induces Apoptosis in CNE1 Nasopharyngeal Carcinoma Cells

Kang Zhu,* Ying He,† Cui Xia,* Jing Yan,* Jin Hou,* Demin Kong,* Yeye Yang,* and Guoxi Zheng*

*Department of Otorhinolaryngology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China
†Department of Radiology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China

Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer, frequently occurring in Southeast Asia and Southern China. Several microRNAs (miRNAs) have been shown to have an inhibitive effect on NPC, while the effect of miR-15a on NPC remains unclear. Thus, our study aimed to investigate the potential effect of miR-15a on NPC cell proliferation, apoptosis, and possible functional mechanism. Human NPC CNE1 cells were transfected with miR-15a mimics, miR-15a inhibitors, or a control. Afterward, cell viability and apoptosis were assayed by using CCK-8, BrdU assay, and flow cytometry. Moreover, Western blot was used to detect the expression changes of proliferation and apoptosis of related proteins. As a result, miR-15a overexpression significantly reduced cell proliferation (p < 0.01 or p < 0.001) and induced cell apoptosis (p < 0.001), while miR-15a suppression got the opposite result for cell proliferation and apoptosis. In addition, miR-15a overexpression upregulated the protein levels of p27, GSK-3β, Bax, procaspase 3, and active caspase 3, whereas miR-15a suppression downregulated these proteins. The protein level of p21 was not significantly regulated by miR-15a overexpression or suppression. These results indicated that miR-15a played a role for inhibition of proliferation and induction of apoptosis in CNE1 cells.

Key words: miR-15a; Nasopharyngeal carcinoma (NPC); Cell proliferation; Apoptosis; GSK-3b; p27

Address correspondence to Guoxi Zheng, Department of Otorhinolaryngology, The Second Affiliated Hospital of Xi’an Jiaotong University, No. 157 Xiwu Road, Xi’an 710004, Shaanxi, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Oncology Research, Vol. 24, pp. 153-160, 2016
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DOI: http://dx.doi.org/10.3727/096504016X14612603423476
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of HPIP Inhibits the Proliferation and Invasion of Head-and-Neck Squamous Cell Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway

Yangjing Chen, Ruimin Zhao, Qian Zhao, Yuan Shao, and Shaoqiang Zhang

Department of Otolaryngology Head and Neck Surgery, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China

Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a corepressor for the transcription factor PBX. Previous studies showed that HPIP is frequently overexpressed in many tumors. However, the role of HPIP in head-and-neck squamous cell carcinoma (HNSCC) has not yet been determined. Thus, we decided to investigate the effects and mechanisms of HPIP in HNSCC. Our results demonstrated that HPIP is highly expressed in human HNSCC cell lines and provides the first evidence that knockdown of HPIP obviously inhibits proliferation and migration/invasion in HNSCC cells in vitro, as well as inhibits tumor growth in vivo. Furthermore, knockdown of HPIP significantly inhibits the expression of p-PI3K and p-Akt in human HNSCC cells. In conclusion, our study demonstrated that knockdown of HPIP significantly inhibits the proliferation and migration/invasion of HNSCC cells by suppressing the PI3K/Akt signaling pathway. Therefore, HPIP may be a novel potential therapeutic target for the treatment of HNSCC.

Key words: Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP); Head-and-neck squamous cell carcinoma (HNSCC); Proliferation; Invasion

Address correspondence to Yangjing Chen, Department of Otolaryngology Head and Neck Surgery, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, China. Tel and Fax: +86-029-85323965; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 161-170, 2016
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DOI: http://dx.doi.org/10.3727/096504016X14618564639178
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells

Li Wan,1 Lin Zhang,1 Kai Fan, Zai-Xing Cheng, Quan-Chao Sun, and Jian-Jun Wang

Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

As a newly identified oncogenic long noncoding RNA (lncRNA), prostate cancer-associated transcript 6 (PCAT6) promoted cellular proliferation and colony formation of prostate cancer. However, the biological function of PCAT6 in lung cancer is still largely unknown. In this study, we found that PCAT6 is significantly increased in cancer tissues compared to normal tissues and positively correlates with metastasis of lung cancer in patients. We then examined PCAT6 expression in lung cancer cell lines and identified that PCAT6 expression was significantly elevated in lung cancer cells compared to normal human bronchial epithelial (NHBE) cells, especially in CL1–5 and H446 cells. PCAT6 knockdown significantly inhibited cellular proliferation and metastasis, as well as induced early apoptosis of lung cancer cells. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation. Finally, a retrospective study further revealed that PCAT6 negatively correlates with overall survival of lung cancer patients. In conclusion, these results suggest that PCAT6 could play an oncogenic role in lung cancer progression and may serve as a biomarker for prognosis of lung cancer patients.

Key words: Long noncoding RNAs (lncRNAs); Prostate cancer-associated transcript 6 (PCAT6); Metastasis; c-Myc; p53; Lung cancer

1These authors provided equal contribution to this work.
Address correspondence to Jian-Jun Wang, M.D., Ph.D., Department of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jie Fang Avenue, Hankou, Wuhan 430030, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 171-179, 2016
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DOI: http://dx.doi.org/10.3727/096504016X14634208142987
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Downregulation of CREB Promotes Cell Proliferation by Mediating G1/S Phase Transition in Hodgkin Lymphoma

Fangjin Lu,*† Ying Zheng,‡ Paul Owusu Donkor,* Peng Zou,§ and Ping Mu†

*Tianjin State Key Laboratory of Modern Chinese Medicine, School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China
†Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Japan
‡Clinical Lab, The Second Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning, China
§Department of Biochemistry and Molecular Biology, Shenyang Medical College, Shenyang, Liaoning, China

The cyclic-AMP response element-binding protein (CREB), a well-known nuclear transcription factor, has been shown to play an essential role in many cellular processes, including differentiation, cell survival, and cell proliferation, by regulating the expression of downstream genes. Recently, increased expression of CREB was frequently found in various tumors, indicating that CREB is implicated in the process of tumorigenesis. However, the effects of CREB on Hodgkin lymphoma (HL) remain unknown. To clarify the role of CREB in HL, we performed knockdown experiments in HL. We found that downregulation of CREB by short hairpin RNA (shRNA) resulted in enhancement of cell proliferation and promotion of G1/S phase transition, and these effects can be rescued by expression of shRNA-resistant CREB. Meanwhile, the expression level of cell cycle-related proteins, such as cyclin D1, cyclin E1, cyclin-dependent kinase 2 (CDK2), and CDK4, was elevated in response to depletion of CREB. Furthermore, we performed chromatin immunoprecipitation (ChIP) assay and confirmed that CREB directly bound to the promoter regions of these genes, which consequently contributed to the regulation of cell cycle. Consistent with our results, a clinical database showed that high expression of CREB correlates with favorable prognosis in B-cell lymphoma patients, which is totally different from the function of CREB in other cancers such as colorectal cancer, acute myeloid leukemia, and some endocrine cancers. Taken together, all of these features of CREB in HL strongly support its role as a tumor suppressor gene that can decelerate cell proliferation by inhibiting the expression of several cell cycle-related genes. Our results provide new evidence for prognosis prediction of HL and a promising therapeutic strategy for HL patients.

Key words: Cyclic-AMP response element-binding protein (CREB); Hodgkin lymphoma (HL); Proliferation; Cell cycle

Address correspondence to Peng Zou, Department of Biochemistry and Molecular Biology, Shen146 Huanghe North Street, Huanggu District, Shenyang 110034, China. Tel: 86-24-62215669; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Ping Mu, Department of Biochemistry, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Tel: 81-52-744-2060; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 181-187, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14635761799038
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells

Mei-han Liu,* Shao-min Shi,† Kai Li,‡ and En-qi Chen*

*Department of Ultrasonography, China–Japan Union Hospital of Jilin University, Changchun, Jilin Province, China
†Department of Respiratory Medicine, China–Japan Union Hospital of Jilin University, Changchun, Jilin Province, China
‡Department of Anesthesia, China–Japan Union Hospital of Jilin University, Changchun, Jilin Province, China

PFTK1 (PFTAIRE protein kinase 1), also named CDK14 (cyclin-dependent kinase 14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is highly expressed in several malignant tumors. However, the role of PFTK1 in the progression of non-small cell lung cancer (NSCLC) is still elusive. In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of PFTK1 endowed NSCLC cells with decreased migration and invasion abilities, as well as epithelial–mesenchymal transition (EMT) progress in A549 cells. A mechanistic study showed that knockdown of PFTK1 inhibited the expression of β-catenin, cyclin D1, and c-Myc in A549 cells. In summary, we report that small interfering RNA (siRNA)-PFTK1 might inhibit the proliferation and invasion of NSCLC cells by suppressing the Wnt/β-catenin signaling pathway. Therefore, PFTK1 may represent a novel therapeutic target for the treatment of NSCLC.

Key words: PFTK1; Non-small cell lung cancer (NSCLC); Invasion; Epithelial–mesenchymal transition (EMT)

Address correspondence to En-qi Chen, Department of Ultrasonography, China–Japan Union Hospital of Jilin University, Changchun 130031, Jilin Province, China. Tel: +86-0431-84995551; Fax: +86-0431-84995551; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 189-196, 2016
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DOI: http://dx.doi.org/10.3727/096504016X14641336229602
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of HVEM, a Lymphocyte Regulator Gene, in Ovarian Cancer Cells Increases Sensitivity to Activated T Cells

Ting Zhang,1 Lei Ye,1 Lingfei Han, Qizhi He, and Jianlong Zhu

Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China

Ovarian cancer is highly malignant with a gradually increasing incidence and a high mortality rate. Immunosuppression is induced in ovarian cancer, although the mechanism detail is not clear. It has been indicated that HVEM (herpesvirus entry mediator) B- and T-lymphocyte attenuator (BTLA) negatively regulates the immune responses of T lymphocytes. Here, HVEM mRNA was found to be elevated in ovarian cancer tissue samples and primary ovarian cancer cells in comparison with benign tissue samples. We then knocked down HVEM expression in an ovarian cancer cell line, OVCAR3, by lentivirus-based small hairpin RNA (shRNA). Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis showed that HVEM-shRNA had no effect on the proliferation, early apoptosis, or cell cycle distribution of OVCAR3. We then isolated activated T cells and performed coculture experiments in Transwell. Remarkably, HVEM-silenced ovarian cancer cells (primary ovarian cancer cells and OVCAR3) increased the number of T cells and the secretion of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), while activated T cells promoted the apoptosis of HVEMsilenced ovarian cancer cells. The current study partially explains the immune escape mechanism of ovarian cancer cells and provides a possible target for immunotherapy.

Key words: Herpesvirus entry mediator (HVEM); Ovarian cancer; T cells; Immunosuppression

1These authors provided equal contribution to this work.
Address correspondence to Jianlong Zhu, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, No. 536 Changle Road, Jing’an District, Shanghai 200040, China. E-mail: jlzhutj@sina.com189


Oncology Research, Vol. 24, pp. 197-204, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14648701447850
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of Upregulated Gene 11 (URG11) Inhibits Proliferation, Invasion, and β-Catenin Expression in Non-Small Cell Lung Cancer Cells

Zhe-liang Liu,* Jiao Wu,† Lin-xian Wang,‡ Jin-feng Yang,† Gao-ming Xiao,* Hui-ping Sun,† and Yue-jun Chen*

*The First Department of Thoracic Surgery, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
†Department of Anesthesiology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China
‡Department of Clinical Laboratory, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China

Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, was found to be involved in the development and progression of several tumors. However, the role of URG11 in human non-small cell lung cancer (NSCLC) has not yet been determined. Therefore, the aim of the present study was to explore the role of URG11 in human NSCLC. Our results found that URG11 was highly expressed in human NSCLC tissues compared with matched normal lung tissues, and higher levels were found in NSCLC cell lines in comparison to the normal lung cell line. Moreover, we also found that knockdown of URG11 significantly inhibited proliferation, migration/invasion of NSCLC cells, as well as suppressed tumor growth in vivo. Furthermore, knockdown of URG11 suppressed the expression of β-catenin, c-Myc, and cyclin D1 in NSCLC cells. Taken together, the study reported here provided evidence that URG11 downregulation suppresses proliferation, invasion, and β-catenin expression in NSCLC cells. Thus, URG11 may be a novel potential therapeutic target for NSCLC.

Key words: Non-small cell lung cancer (NSCLC); Upregulated gene 11 (URG11); Proliferation; Invasion; Wnt/β-catenin signaling pathway

Address correspondence to Jiao Wu, Department of Anesthesiology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410006, China. Tel: +86-0731-89762510; Fax: +86-0731-89762510; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 24, pp. 205-214, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14648701447896
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Knockdown of Zinc Transporter ZIP5 by RNA Interference Inhibits Esophageal Cancer Growth In Vivo

Qian
Li, Jing Jin, Jianghui Liu, Liqun Wang, and Yutong He Cancer Institute, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China

We recently found that SLC39A5 (ZIP5), a zinc transporter, is overexpressed in esophageal cancer. Downregulation of ZIP5 inhibited the proliferation, migration, and invasion of the esophageal cancer cell line KYSE170 in vitro. In this study, we found that downregulation of SLC39A5 (ZIP5) by interference resulted in a significant reduction in esophageal cancer tumor volume and weight in vivo. COX2 (cyclooxygenase 2) expression was decreased and E-cadherin expression was increased in the KYSE170K xenografts, which was caused by the downregulation of ZIP5. However, we did not find that the downregulation of ZIP5 caused a change in the relative expressions of cyclin D1, VEGF (vascular endothelial growth factor), MMP9 (matrix metalloprotein 9), and Bcl-2 (B-cell lymphoma/leukmia-2) mRNA or an alteration in the average level of zinc in the peripheral blood and xenografts in vivo. Collectively, these findings indicate that knocking down ZIP5 by small interfering RNA (siRNA) might be a novel treatment strategy for esophageal cancer with ZIP5 overexpression.

Key words: SLC39A5 (ZIP5); Esophageal cancer; COX2; E-cadherin; Xenograft; Zinc

Address correspondence to Professor Yutong He, Cancer Institute, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, China. Tel: +86-0311-86095613; Fax: +86-0311-86095613; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it