Inhibition of proliferation and induction of apoptosis by trimethoxyl stilbene (TMS) in a lung cancer cell line

• Published in: Asian Pacific journal of cancer prevention : APJCP Vol. 12; no. 9; p. 2263
• Main Authors: Liu, Ping, Wang, Xin, Hu, Chunhong, Hu, Tiehui
• Format: Journal Article
• Language: English
• Published: Thailand 2011
• Subjects: Adenocarcinoma - drug therapy; Adenocarcinoma - metabolism; Apoptosis - drug effects; Apoptosis - genetics; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - metabolism; Carcinoma, Non-Small-Cell Lung - pathology; Caspase 3 - genetics; Caspase 3 - metabolism; Cell Line, Tumor; Cell Proliferation - drug effects; Down-Regulation - drug effects; Humans; I-kappa B Proteins - genetics; I-kappa B Proteins - metabolism; Janus Kinase 2 - genetics; Janus Kinase 2 - metabolism; Lung Neoplasms - drug therapy; Lung Neoplasms - genetics; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; NF-kappa B - genetics; NF-kappa B - metabolism; Signal Transduction - drug effects; Signal Transduction - genetics; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism; STAT5 Transcription Factor - genetics; STAT5 Transcription Factor - metabolism; Stilbenes - pharmacology; Up-Regulation - drug effects
• ISSN: 2476-762X

Trimethoxyl stilbene (TMS) is a derivative of resveratrol, a compound shown to inhibit development of a variety of tumor types. We aimed to evaluate the effect of TMS on cell proliferation and apoptosis in the A549 non-small cell lung cancer cell line. Growth inhibition rate and colony formation was measured and apoptosis was determined with Hoechst 33258 staining. Protein expression levels of caspase-3, STAT3, STAT5b, JAK2, NF-κB, and IκB were examined by Western blotting. Furthermore, localization of NF-κB protein was also explored. TMS inhibited proliferation (IC50 8.6 μmol/L) and induced apoptosis of the cells in a concentration-dependent manner., also inducing apoptosis accompanied by up-regulated expression and cleavage activation of caspase-3, up-regulation of IκB and down-regulation of NFκB, STAT3, STAT5b, and JAK2 signal transduction. TMS has potential as a new drug for treatment of non-small cell lung cancer patients with anti-proliferation and apoptosis inducing effect of TMS to A549 cells apparently related to its inhibitory effect on STATs and NF-κB signal transduction. Up-regulation of caspase-3 further supports the potential clinical use of TMS for the treatment of non-small cell lung adenocarcinoma.