Abstract | BACKGROUND: METHODS:
Gastric cancer cell lines and clinical tumor samples were used to assess FGD5-AS1 expression levels. Lentivirus containing FGD5-AS1 small interfering RNA (sh-FGD5AS1) was applied to knockdown FGD5-AS1 expression. Cancer cells in vitro and in vivo proliferation, and 5-FU chemoresistance were assessed, respectively. Expressions of hsa-miR-153-3p/CITED2 were also assessed in FGD5-AS1-downregulated gastric cancer cells. Hsa-miR-153-3p was knocked down and CITED2 was upregulated to assess their direct functional correlations with FGD5-AS1 in gastric cancer. RESULTS: Both gastric cancer cell lines and human tumor samples showed aberrant FGD5-AS1 upregulation. Lentiviral-induced FGD5-AS1 knockdown reduced cancer proliferation, 5-FU chemoresistance in vitro, and tumorigenicity in vivo. Hsa-miR-153-3p/CITED2 axis was confirmed to be downstream of FGD5-AS1 in gastric cancer. Hsa-miR-153-3p inhibition or CITED2 upregulation reversed the tumor-suppressing effects of FGD5-AS1 downregulation on gastric cancer proliferation and 5-FU chemoresistance. CONCLUSION: We demonstrated that FGD5-AS1 can regulate human gastric cancer cell functions, possibly through its downstream epigenetic axis of hsa-miR-153-3p/CITED2.
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Authors | Yunhan Gao, Mubing Xie, Yi Guo, Qian Yang, Song Hu, Zhongfu Li |
Journal | Frontiers in genetics
(Front Genet)
Vol. 11
Pg. 715
( 2020)
ISSN: 1664-8021 [Print] Switzerland |
PMID | 32849774
(Publication Type: Journal Article)
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Copyright | Copyright © 2020 Gao, Xie, Guo, Yang, Hu and Li. |