Effect and mechanism of long-chain non-coding RNA FAM83H-AS1 on cell cycle, proliferation and metastasis of gastric cancer

Acta Universitatis Medicinalis Anhui 2020 09 v.55 1327-1331     font:big middle small

Found programs:

Authors:Wang Tao; Ma Muyuan; Ye Xiaofeng

Keywords:gastric cancer;lncRNA FAM83H-AS1;cell cycle;proliferation;metastasis;epithelial-mesenchymal transition

DOI:10.19405/j.cnki.issn1000-1492.2020.09.003

〔Abstract〕 Objective To study the effect of long non-coding RNA family with sequence similarity 83 member H antisense RNA 1(lncRNA FAM83 H-AS1) on cell cycle, proliferation and metastasis of gastric cancer cells, and explore its possible mechanisms. Methods qRT-PCR was used to detect the expression level of FAM83 H-AS1 in gastric cancer cell lines MKN-45, SGC-7901, MGC-803 and human immortalized normal gastric epithelial cell line GES-1. The highest expression of gastric cancer cell line was selected for FAM83 H-AS1 siRNA infection, which was divided into si-NC group and si-FAM83 H-AS1 group. The expression of FAM83 H-AS1 in each group was detected by qRT-PCR. The effect of FAM83 H-AS1 on cell cycle was detected by flow cytometry. The effect of FAM83 H-AS1 on cell proliferation was detected by MTS and plate cloning assay. The effect of FAM83 H-AS1 on cell metastasis ability was detected by Transwell assay. Western blot was used to detect the effect of FAM83 H-AS1 on the expression of cyclinD1 and cyclin dependent kinase 4(CDK4) and epithelial-mesenchymal transition(EMT) marker proteins. Results The results of qRT-PCR showed that the expression level of FAM83 H-AS1 in gastric cancer cell lines was higher than that in human immortalized normal gastric epithelial cell line GES-1(P<0.05), and the gastric cancer cell line MKN-45 with the highest FAM83 H-AS1 expression level was selected to transfect FAM83 H-AS1 siRNA. qRT-PCR results showed that the expression of FAM83 H-AS1 decreased in si-FAM83 H-AS1 cells(P<0.05), the proliferation and metastasis ability and the expression of cyclinD1 and CDK4 proteins in si-FAM83 H-AS1 group MKN-45 cells decreased, the expression of EMT marker protein E-cadherin protein increased, and the expression of N-cadherin and Vinmentin protein decreased. Conclusion Interference with the expression of FAM83 H-AS1 inhibits the proliferation and metastasis of gastric cancer cells. FAM83 H-AS1 may be a novel target for the treatment of gastric cancer.