TY - JOUR T1 - Tranilast Inhibits TGF-β1–induced Epithelial-mesenchymal Transition and Invasion/Metastasis <em>via</em> the Suppression of Smad4 in Human Lung Cancer Cell Lines JF - Anticancer Research JO - Anticancer Res SP - 3287 LP - 3296 DO - 10.21873/anticanres.14311 VL - 40 IS - 6 AU - KOJI TAKAHASHI AU - TOSHI MENJU AU - SHIGETO NISHIKAWA AU - RYO MIYATA AU - SATONA TANAKA AU - YOJIRO YUTAKA AU - YOSHITO YAMADA AU - DAISUKE NAKAJIMA AU - MASATSUGU HAMAJI AU - AKIHIRO OHSUMI AU - TOYOFUMI FENGSHI CHEN-YOSHIKAWA AU - TOSHIHIKO SATO AU - MAKOTO SONOBE AU - HIROSHI DATE Y1 - 2020/06/01 UR - http://ar.iiarjournals.org/content/40/6/3287.abstract N2 - Background/Aim: Transforming growth factor β1 (TGF-β1) is an important epithelial-mesenchymal transition (EMT) activator that regulates the expression of E-cadherin and vimentin through Smad signalling. Tranilast is an anti-allergic drug that inhibits TGF-β1, and is used in the treatment of keloids and hypertrophic scars. We investigated whether tranilast inhibits TGF-β1-induced EMT and invasiveness in human non-small cell lung cancer cell lines. Materials and Methods: We examined the effects of tranilast treatment on EMT markers, TGF-β1/Smad signalling, and cell invasiveness in A549 and PC14 cells. Tumours from a mouse orthotopic lung cancer model with or without tranilast treatment were also immunohistochemically evaluated. Results: Tranilast increased E-cadherin expression via Smad4 suppression and inhibited cell invasion in TGF-β1-stimulated cells. Tranilast treatment of the in vivo mouse model reduced the pleural dissemination of cancer cells and suppressed vimentin and Smad4 expression. Conclusion: Tranilast inhibited TGF-β1-induced EMT and cellular invasion/metastasis by suppressing Smad4 expression in cancer cells. ER -