Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Role of OCT4 in cisplatin treatment of testicular embryonal carcinoma

Qin Le^1,2, Jie Lin^1,2, Xiaoxiao Xie³, Xiangbo Yu², Yang Cai⁴, Yangping Shentu⁵, Aihua Zhang⁶ , Aiwu Li⁷

¹Department of Pediatric Surgery, Qilu Hospital, Shandong University, Jinan, 250012; ²Department of Pediatric Surgery; ³Department of Medical Imaging, The Second Affiliated Hospital and Yuying Childrenâ€™s Hospital of Wenzhou Medical University, Wenzhou 325027; ⁴Department of Urology, Qingtian People's Hospital, Qingtian 323000; ⁵Wenzhou Medical University, Medical Function Center, Wenzhou 325000; ⁶Animal Experiment Center of Scientific Research; ⁷Department of Pediatric Surgery, Qilu Hospital, Shandong University, Jinan 250012, China.

For correspondence:- Aiwu Li Email: liaiwuxwymed@163.com

Accepted: 27 June 2018 Published: 28 July 2018

Citation: Le Q, Lin J, Xie X, Yu X, Cai Y, Shentu Y, et al. Role of OCT4 in cisplatin treatment of testicular embryonal carcinoma. Trop J Pharm Res 2018; 17(7):1353-1360 doi: 10.4314/tjpr.v17i7.18

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the role of embryonal transcription factor OCT4 in cisplatin treatment of testicular embryonal carcinoma.

Methods: In vitro assays were employed to assess the effect of cisplatin treatment on testicular embryonal carcinoma cell lines under OCT4 silencing. Following treatment with 500 ng/μL cisplatin, MTT assay was used to examine cell proliferation of 2012-EP and 833K-E cells with or without OCT silencing, while wound healing assay was used to examine cell migration ability. Transwell assay and crystal violet staining were employed to measure cell invasive capacity, whereas the distribution pattern of cell cycle was assessed by flow cytometry. The expression levels of several critical components in tumorigenicity related pathways with or without OCT silencing were determined by Western-blot analysis.

Results: Cisplatin enhanced OCT4-silenced cell viability at all concentration (p < 0.01) when compared to control cells. Upon treatment with 500 ng/μL cisplatin, OCT4-silenced cells showed 2- to 3-fold enhancement in cell proliferation (p < 0.001), 2-fold increase in cell migration capacity (p < 0.001), and about 1.5-fold enhancement in invasive capacity (p < 0.001) when compared to control cells. In addition, OCT4 silencing upregulated the expression level of the proteins involved in cell proliferation, cell mobility, cancer metastasis and cell cycle control.

Conclusion: The results suggest that OCT4 may serve as a therapeutic target for testicular embryonal carcinoma treatment in combination with cisplatin by modulating OCT4 expression level. This physiological evidence indicates that OCT4 downregulation contributes to cisplatin resistance in chemotherapy and subsequent disease relapse.

Keywords: OCT4, Cisplatin resistance, Testicular embryonal carcinoma, Chemotherapy