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Potential targets of TMEM176A in the growth of glioblastoma cells

Authors Liu Z, An H, Song P, Wang D, Li S, Chen K, Pang Q

Received 10 July 2018

Accepted for publication 21 September 2018

Published 2 November 2018 Volume 2018:11 Pages 7763—7775

DOI https://doi.org/10.2147/OTT.S179725

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche


Zhiguo Liu,1 Haixia An,2 Peng Song,3 Dejing Wang,4 Shichun Li,5 Kai Chen,6 Qi Pang7

1Department of Neurosurgery, People’s Hospital of Zhangqiu, Shandong Provincial Hospital Affiliated to Shandong University, Zhangqiu, Jinan, Shandong 250200, People’s Republic of China; 2Department of Oncology, Jinan Zhangqiu Hospital of Traditional Chinese Medicine, Zhangqiu, Jinan, Shandong 250200, People’s Republic of China; 3Department of Orthopedics, People’s Hospital of Zhangqiu, Zhangqiu, Jinan, Shandong 250200, People’s Republic of China; 4Department of Stomatology, People’s Hospital of Zhangqiu, Zhangqiu, Jinan, Shandong 250200, People’s Republic of China; 5Department of Doppler Ultrasonic, People’s Hospital of Zhangqiu, Zhangqiu, Jinan, Shandong 250200, People’s Republic of China; 6Department of Neurology, The Fourth People’s Hospital of Jinan, Tianqiao, Jinan, Shandong 250200, People’s Republic of China; 7Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Huaiyin, Jinan, Shandong 250200, People’s Republic of China

Background: Human transmembrane protein 176A (TMEM176A) is upregulated in several tumors. Growing evidence has suggested the high clinical value of TMEM176A as a biomarker for early tumor diagnosis. However, less is known about the function of TMEM176A in glioblastomas (GBMs).
Methods: In this study, we systematically analyzed the effect of TMEM176A knockdown and overexpression in GBM cells (U87, T98G and A172) on cell proliferation, cell cycle and cell apoptosis.
Results: Our results indicated that TMEM176A acted as a tumor-promoting factor in GBM cells. Moreover, a specific ERK1/2 inhibitor, U0126, suppressed the function of TMEM176A in GBM cells. Therefore, we proposed that TMEM176A may be involved in a pathway including ERK1/2 in the regulation of the cell cycle. Moreover, we also found that TMEM176A affected the expression of Bcl2 and played a central role in apoptosis of GBM cells.
Conclusion: Taken together, our results not only elucidated the multiple functions of TMEM176A in GBM cells but also provided a deep insight into the potential targets of TMEM176A in the growth of GBM cells.

Keywords: TMEM176A, cell cycle, cell apoptosis, ERK1/2, glioblastomas

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