Abstract | BACKGROUND: METHODS: We assessed expression and biological behavior of OPCML in gastric cancer. RESULTS: OPCML expression was markedly reduced in tumor tissues and cancer cell lines. Decreased OPCML expression had a significant association with unfavorable tumor stage (p = 0.007) and grading (p < 0.001). Furthermore, the results revealed that OPCML was an independent prognostic factor for overall survival in gastric cancer (p = 0.002). In addition, ectopic expression of OPCML in cancer cells significantly inhibited cell viability (p < 0.01) and colony formation (p < 0.001), arrest cell cycle in G0/G1 phase and induced apoptosis, and suppressed tumor formation in nude mice. The alterations of phosphorylation status of AKT and its substrate GSK3β, up-regulation of pro-apoptotic regulators including caspase-3, caspase-9 and PARP, and up-regulation of cell cycle regulator p27, were implicated in the biological activity of OPCML in cancer cells. CONCLUSION: Down-regulated OPCML expression might serve as an independent predictor for unfavorable prognosis of patients, and the biological behavior supports its role as a tumor suppressor in gastric cancer.
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Authors | Xiangbin Xing, Weibin Cai, Sanmei Ma, Yongfei Wang, Huijuan Shi, Ming Li, Jinxia Jiao, Yang Yang, Longshan Liu, Xiangliang Zhang, Minhu Chen |
Journal | BMC cancer
(BMC Cancer)
Vol. 17
Issue 1
Pg. 268
(Apr 14 2017)
ISSN: 1471-2407 [Electronic] England |
PMID | 28407749
(Publication Type: Journal Article)
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Chemical References |
- Cell Adhesion Molecules
- GPI-Linked Proteins
- OPCML protein, human
- GSK3B protein, human
- Glycogen Synthase Kinase 3 beta
- Proto-Oncogene Proteins c-akt
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Topics |
- Animals
- Cell Adhesion Molecules
(genetics, metabolism)
- Cell Line, Tumor
- Cell Survival
- Disease Progression
- Down-Regulation
- Female
- GPI-Linked Proteins
(genetics, metabolism)
- Gene Expression Regulation, Neoplastic
- Glycogen Synthase Kinase 3 beta
(metabolism)
- Humans
- Male
- Mice
- Neoplasm Transplantation
- Prognosis
- Proto-Oncogene Proteins c-akt
(metabolism)
- Signal Transduction
- Stomach Neoplasms
(genetics, metabolism, pathology)
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