Open Access
ARTICLE
CSTB Downregulation Promotes Cell Proliferation and Migration and Suppresses Apoptosis in Gastric Cancer SGC-7901 Cell Line
Jian Zhang*1, ZhenFeng Shi†1, JinXing Huang‡, XiaoGuang Zou§
* Department of Cancer Center, The First People’s Hospital of Kashi Prefecture, Kashi Prefecture, Xinjiang, P.R. China
† Department of Urology Surgery Center, The People’s Hospital of Xinjiang Uyghur Autonomous Region, Xinjiang, P.R. China
‡ Department of Urinary Surgery, The People’s Hospital of Shache County, Xinjiang, P.R. China
§ The First People’s Hospital of Kashi Prefecture, Xinjiang, P.R. China
1
These authors are co-first authors in this study.
Oncology Research 2016, 24(6), 487-494. https://doi.org/10.3727/096504016X14685034103752
Abstract
This study aimed to investigate the pivotal role of cystatin B (CSTB) in the development of gastric cancer and
to explore its possible regulatory mechanism. Human gastric cancer SGC-7901 cells as a model in vitro were
transfected with plasmid PCDNA3.1-CSTB and siRNA-CSTB using Lipofectamine 2000. Quantitative realtime PCR (qRT-PCR) and Western blotting were performed to determine the relative expression of CSTB and
PI3K/Akt/mTOR pathway-related protein. Moreover, MTT assay, Transwell assay, and flow cytometry were
used to assess cell proliferation, migration, and apoptosis, respectively. The results showed that CSTB was
significantly downregulated in SGC-7901 cells compared with gastric epithelial cells. CSTB was successfully
overexpressed and suppressed after cells were transfected with pc-CSTB and si-CSTB, respectively. Moreover,
cell viability and migration were significantly decreased after being transfected with pc-CSTB when compared
with the control group, while being obviously increased after transfection with si-CSTB. However, cell apoptosis was significantly induced after being transfected with pc-CSTB, while being obviously suppressed after
transfection with si-CSTB. Besides, the expression levels of p-PI3K, p-Akt, and p-mTOR proteins were all
significantly decreased in the pc-CSTB transfection group when compared with the control group, while being
increased in the si-CSTB transfection group. Our findings suggest that CSTB downregulation may promote the
development of gastric cancer by affecting cell proliferation and migration, and the PI3K/Akt/mTOR signaling pathway was activated in this process. CSTB may serve as a potential therapeutic target for gastric cancer.
Keywords
Cite This Article
APA Style
Zhang, J., Shi, Z., Huang, J., Zou, X. (2016). CSTB downregulation promotes cell proliferation and migration and suppresses apoptosis in gastric cancer SGC-7901 cell line. Oncology Research, 24(6), 487-494. https://doi.org/10.3727/096504016X14685034103752
Vancouver Style
Zhang J, Shi Z, Huang J, Zou X. CSTB downregulation promotes cell proliferation and migration and suppresses apoptosis in gastric cancer SGC-7901 cell line. Oncol Res. 2016;24(6):487-494 https://doi.org/10.3727/096504016X14685034103752
IEEE Style
J. Zhang, Z. Shi, J. Huang, and X. Zou "CSTB Downregulation Promotes Cell Proliferation and Migration and Suppresses Apoptosis in Gastric Cancer SGC-7901 Cell Line," Oncol. Res., vol. 24, no. 6, pp. 487-494. 2016. https://doi.org/10.3727/096504016X14685034103752