RT Journal Article
SR Electronic
T1 The Antitumor Effects of Metformin on Gastric Cancer <em>In Vitro</em> and on Peritoneal Metastasis
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 6263
OP 6269
DO 10.21873/anticanres.12982
VO 38
IS 11
A1 NOBUFUMI SEKINO
A1 MASAYUKI KANO
A1 YASUNORI MATSUMOTO
A1 HARUHITO SAKATA
A1 KENTARO MURAKAMI
A1 TAKESHI TOYOZUMI
A1 RYOTA OTSUKA
A1 MASAYA YOKOYAMA
A1 TADASHI SHIRAISHI
A1 KOICHIRO OKADA
A1 TOSHIKI KAMATA
A1 TAKAHIRO RYUZAKI
A1 HISAHIRO MATSUBARA
YR 2018
UL http://ar.iiarjournals.org/content/38/11/6263.abstract
AB Background/Aim: Gastric cancer (GC) with peritoneal metastasis remains difficult to treat. The anti-diabetic drug metformin exerts various antitumor effects via the 5’-adenosine monophosphate-activated protein kinase (AMPK) pathway and nuclear factor-kappa B (NF-ĸB). Therefore, we evaluated the antitumor effects of metformin for GC in vitro and on peritoneal metastasis. Materials and Methods: The human GC cell lines MKN1, MKN45, KATO-III and SNU-1 were used. The antiproliferative effect was evaluated in vitro with 0.5 mM or 25 mM glucose and in vivo using tumor xenograft peritoneal models of metastasis. The protein expression of AMPK, liver kinase B1 (LKB1) and NF-ĸB in tumors was examined by western blotting. Results: Metformin inhibited cell proliferation in all GC lines and sensitivity was increased under low-glucose conditions in vitro. Metformin also suppressed peritoneal metastasis. In tumors, metformin reduced the numbers of proliferating cells and NF-ĸB expression, but a similar trend was not noted for AMPK. Conclusion: Metformin may be a useful drug for the treatment of GC with peritoneal metastasis.