Open AccessAntihypertensive drug telmisartan inhibits cell proliferation of gastrointestinal stromal tumor cells in vitro
Author(s) -
Hideki Kobara,
Shintaro Fujihara,
Hisakazu Iwama,
Takanori Matsui,
Ayako Fujimori,
Taiga Chiyo,
Tingting Shi,
Nobuya Kobayashi,
Noriko Nishiyama,
Tatsuo Yachida,
Tomoko Tadokoro,
Kyoko Oura,
Joji Tani,
Koji Fujita,
Takako Nomura,
Hirohito Yoneyama,
Asahiro Morishita,
Keiichi Okano,
Yasuyuki Suzuki,
Hideki Mori,
Tsutomu Masaki
Publication year - 2020
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2020.11144
Subject(s) - telmisartan , cell cycle , candesartan , cancer research , cell growth , angiotensin ii , stromal cell , cell , imatinib , pharmacology , medicine , cancer , biology , endocrinology , receptor , biochemistry , myeloid leukemia , blood pressure
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract. The angiotensin II type 1 receptor blockers, telmisartan and candesartan, are widely used antihypertensive drugs that inhibits cancer cell proliferation; however, its underlying mechanisms in mesenchymal tumors, including GIST, remains unknown. The present study aimed to investigate the effect of telmisartan on GIST‑T1 cells and its underlying mechanism. Telmisartan and candesartan inhibited the proliferation of these cells by blocking the G0 to G1 cell cycle transition, which was accompanied by a decrease in cell cycle‑related proteins such as cyclin D1. Furthermore, telmisartan exposure significantly altered microRNA expression in vitro. In conclusion, telmisartan suppressed human GIST cell proliferation by inducing cell cycle arrest in vitro.