PMID- 30988743 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20200929 IS - 1792-0981 (Print) IS - 1792-1015 (Electronic) IS - 1792-0981 (Linking) VI - 17 IP - 5 DP - 2019 May TI - Effect of T-cadherin on the AKT/mTOR signaling pathway, gastric cancer cell cycle, migration and invasion, and its association with patient survival rate. PG - 3607-3613 LID - 10.3892/etm.2019.7350 [doi] AB - Gastric cancer (GC) is among the most common types of human cancer and is associated with recurrence and metastasis, despite comprehensive surgical and medical treatment. Previous studies observed downregulation of T-cadherin expression in GC tissues, suggesting that this protein may act as an oncosuppressor. The current study investigated the activity of T-cadherin in GC tissues. In a follow-up study of 81 patients with GC, a Kaplan-Meier analysis of overall survival revealed a strong association of T-cadherin overexpression with increased overall survival (P<0.01). Furthermore, stable T-cadherin-overexpressing cell lines were established from HGC-27 cells via transfection of a pcDNA3.1-T-cadherin plasmid and in vitro growth and cell cycle of these cells were measured using MTT and flow cytometry assays, respectively. MTT assays revealed that proliferation of engineered T-cadherin-overexpressing cells was significantly inhibited and flow cytometry demonstrated that T-cadherin overexpression in HGC-27 cells induced cell cycle arrest in the G(0)/G(1) phase. Transwell assays demonstrated that T-cadherin-overexpressing HGC-27 cells exhibited reduced invasiveness and metastatic potential. Phosphorylated (p)-protein kinase B (AKT) and p-mammalian target of rapamycin (mTOR) protein levels were reduced in T-cadherin overexpressing HGC-27 cells, suggesting that the AKT/mTOR signaling pathway was involved in the gastric tumor inhibitory effect of T-cadherin. Administration of AKT-activator, insulin-like growth factor-1, to T-cadherin-overexpressing HGC-27 cells significantly affected the proliferation phenotype. In conclusion, the current study provided clinical evidence and revealed a potential mechanism supporting that T-cadherin inhibits gastric tumorigenesis through inhibition of the AKT/mTOR signaling pathway. FAU - Lin, Jianqing AU - Lin J AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Chen, Zhiyao AU - Chen Z AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Huang, Zhijun AU - Huang Z AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Chen, Feng AU - Chen F AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Ye, Zeyi AU - Ye Z AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Lin, Shaoze AU - Lin S AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. FAU - Wang, Weidong AU - Wang W AD - Department of Surgical Oncology, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, P.R. China. LA - eng PT - Journal Article DEP - 20190306 PL - Greece TA - Exp Ther Med JT - Experimental and therapeutic medicine JID - 101531947 PMC - PMC6447793 OTO - NOTNLM OT - T-cadherin OT - gastric cancer OT - invasion OT - migration OT - overexpression EDAT- 2019/04/17 06:00 MHDA- 2019/04/17 06:01 PMCR- 2019/03/06 CRDT- 2019/04/17 06:00 PHST- 2017/11/04 00:00 [received] PHST- 2019/01/03 00:00 [accepted] PHST- 2019/04/17 06:00 [entrez] PHST- 2019/04/17 06:00 [pubmed] PHST- 2019/04/17 06:01 [medline] PHST- 2019/03/06 00:00 [pmc-release] AID - ETM-0-0-7350 [pii] AID - 10.3892/etm.2019.7350 [doi] PST - ppublish SO - Exp Ther Med. 2019 May;17(5):3607-3613. doi: 10.3892/etm.2019.7350. Epub 2019 Mar 6.