A 12-year experience in the treatment of gastric cancer. Long-term follow-up and survival analyses at 5 and 10 years

Gjoni, Elson; Zurleni, Tommaso; Cassiano, A.; Ballabio, Andrea; Olmetti, S.; Ceriani, Paola; Are, F.; Carsenzuola, V.; Marzoli, L.; Zurleni, F.

doi:10.1016/j.ejso.2012.07.040

Cited by 1 publication

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“…Approximately 400,000 people have been diagnosed with GC, and the mortality rate is as high as 70%–75% annually in China 2,3 . Although the standard of diagnosis and treatment of GC have continuously improved, the percentage of 5-year survival is still unsatisfactory 4 . The mechanism of GC is complex and multifactorial, and many factors are implicated in these processes 5 .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA 495 Inhibits Proliferation and Metastasis and Promotes Apoptosis by Targeting Twist1 in Gastric Cancer Cells

et al. 2019

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Recently, microRNAs (miRNAs) have reported to participate in multiple biological processes. However, the effects of miR-495 on gastric cancer (GC) remain unclear. The purpose of this study is to explore the functions of miR-495 in GC cells proliferation, metastasis and apoptosis. SGC-7901 and BGC-823 were transfected with miR-495 mimic, miR-495 inhibitor and negative controls (mimic control and inhibitor control). The expressions of miR-495, cell viability, migration, apoptosis and apoptosis-related factors were examined by qRT-PCR, trypan blue staining, Transwell, flow cytometry and western blot, respectively. Simultaneously, the key factors expressions of EMT were detected by qRT-PCR again. The direct target gene of miR-495 was confirmed by dual luciferase assay. Additionally, sh-Twist1, pc-Twist1 and corresponding control were also transfected into SGC-7901 and BGC-823 cells, and then the protein levels of EMT-associated factors were detected by western blot. MiR-495 was down-regulated in GC cells. MiR-495 expression level was effectively overexpressed or suppressed in SGC-7901 and BGC-823 cells. Overexpression of miR-495 significantly decreased cell viability, migration and increased apoptosis as well as inhibited EMT process. Suppression of miR-495 showed contrary results. Twist1 was clarified as a target gene of miR-495, and Twist1 silencing obviously reduced the promotion effect of miR-495 suppression on these biological processes. Besides, Twist1 silencing significantly blocked EMT signal pathway in both SGC-7901 and BGC-823 cells. MiR-495 inhibited proliferation, metastasis and promoted apoptosis by targeting Twist1 in GC cells. These data indicated that miR-495 might be a novel anti-tumor factor of GC and provide a new method for treatment of GC.

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Section: Introductionmentioning

confidence: 99%