Inhibition of apoptosis by miR‑122‑5p in α‑fetoprotein‑producing gastric cancer
Author(s) -
Suguru Maruyama,
Shinji Furuya,
Kensuke Shiraishi,
Hiroki Shimizu,
Ryo� Saito,
Hidenori Akaike,
Naohiro Hosomura,
Yoshihiko Kawaguchi,
Hidetake Amemiya,
Hiromichi Kawaida,
Makoto Sudo,
Shingo Inoue,
Hiroshi Kono,
Daisuke Ichikawa
Publication year - 2019
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2019.7023
Subject(s) - oncogene , apoptosis , molecular medicine , cancer , cancer research , cell cycle , biology , blot , foxo3 , mir 122 , cell culture , microrna , gene , protein kinase b , biochemistry , genetics
α‑Fetoprotein (AFP)‑producing gastric cancer (AFPGC) is recognized as one of the most aggressive tumors with subsequent poor prognosis compared with common gastric cancer (GC) subtypes. However, the molecular mechanism remains to be elucidated. We previously identified that miR‑122‑5p could be a useful biomarker in AFPGC patients. We examined herein the biological function of miR‑122‑5p and the molecular mechanism underlying tumor progression in AFPGC. We used the AFPGC cell line (FU97) and miR‑122‑5p inhibitor to examine the function of miR‑122‑5p. Moreover, we investigated the possible targets of miR‑122‑5p. The expression level of miR‑122‑5p was significantly increased in the FU97 cell line than in common GC cell lines. Also, suppression of miR‑122‑5p significantly reduced AFP levels and proliferation in AFPGC through an induction of apoptosis. Western blotting revealed that the expression of anti‑apoptotic protein (Bcl‑2) was decreased and that of pro‑apoptotic protein (caspase‑3) was increased in miR‑122‑5p suppression of FU97. Moreover, we revealed that FOXO3 was an important target of miR‑122‑5p in AFPGC, which inhibited apoptosis and subsequently manifested aggressiveness. In conclusion, miR‑122‑5p inhibited apoptosis and facilitated tumor progression by targeting FOXO3 in AFPGC, which indicates the possibility of miR‑122‑5p as a potential therapeutic target in AFPGC.
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