Observational Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 7, 2016; 22(45): 10053-10063
Published online Dec 7, 2016. doi: 10.3748/wjg.v22.i45.10053
Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression
Jing-Ran Su, Jing-Hua Kuai, Yan-Qing Li
Jing-Ran Su, Yan-Qing Li, Department of Gastroenterology, Laboratory of Translational Gastroenterology, Shandong University, Qilu Hospital, Jinan 250012, Shandong Province, China
Jing-Hua Kuai, Department of Gastroenterology, Shandong University, Qilu Hospital of Shandong University (Qingdao), Qingdao 266035, Shandong Province, China
Author contributions: Su JR designed the study, performed the majority of experiments and wrote the manuscript; Kuai JH provided analytical tools and was also involved in editing of the manuscript; Li YQ co-ordinated and provided the collection of all human materials, in addition to providing financial support for this work.
Supported by National Natural Science Foundation of China, No. 81330012.
Institutional review board statement: The study was reviewed and approved by the Medical Ethics Committee of Shandong Provincial Hospital.
Informed consent statement: The authors of this paper guarantee that all study participants or their legal guardian provided informed written consent about personal and medical data collection prior to study enrollment.
Conflict-of-interest statement: There are no conflicts of interest in relation to this manuscript.
Data sharing statement: There are no additional data available in relation to this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Yan-Qing Li, MD, PhD, Department of Gastroenterology, Laboratory of Translational Gastroenterology, Shandong University, Qilu Hospital, 107 Wenhuaxi Road, Jinan 250012, Shandong Province, China. liyanqing@sdu.edu.cn
Telephone: +86-531-82166090 Fax: +86-531-82166090
Received: August 1, 2016
Peer-review started: August 2, 2016
First decision: August 19, 2016
Revised: September 7, 2016
Accepted: October 26, 2016
Article in press: October 26, 2016
Published online: December 7, 2016
Processing time: 126 Days and 21.6 Hours
Abstract
AIM

To determine the influence of Smoc2 on hepatocellular carcinoma (HCC) cell proliferation and to find a possible new therapeutic target for preventing HCC progression.

METHODS

We detected expression of Smoc2 in HCC tissues and corresponding non-tumor liver (CNL) tissues using PCR, western blot, and immunohistochemistry methods. Subsequently, we down-regulated and up-regulated Smoc2 expression using siRNA and lentivirus transfection assay, respectively. Then, we identified the effect of Smoc2 on cell proliferation and cell cycle using CCK-8 and flow cytometry, respectively. The common cell growth signaling influenced by Smoc2 was detected by western blot assay.

RESULTS

The expression of Smoc2 was significantly higher in HCC tissues compared with CNL tissues. Overexpression of Smoc2 promoted HCC cell proliferation and cell cycle progression. Down-regulation of Smoc2 led to inhibition of cell proliferation and cell cycle progression. Smoc2 had positive effect on ERK and AKT signaling.

CONCLUSION

Smoc2 promotes the proliferation of HCC cells through accelerating cell cycle progression and might act as an anti-cancer therapeutic target in the future.

Keywords: Smoc2; Hepatocellular carcinoma; Cell cycle; Proliferation

Core tip: In our study, we confirmed that Smoc2 was up-regulated in hepatocellular carcinoma (HCC) tissues and played an important role in regulating liver cancer cell proliferation. Besides, we verified that Smoc2 participated in promoting HCC cell proliferation mainly through regulation of cell cycle progression. We have not investigated the promotive role of Smoc2 in regulating cell proliferation, whether it is through cell cycle regulation only or involves regulation of cell apoptosis as well. Moreover, the exact mechanism of how Smoc2 regulates cell cycle remains unclear. The core contents of our study included Smoc2 promotion of HCC cell proliferation via accelerating cell cycle progression.