Open AccessAbsence of STAT1 disturbs the anticancer effect induced by STAT3 inhibition in head and neck carcinoma cell lines
Author(s) -
So Yeon Shim,
MyungWhun Sung,
Seok-Woo Park,
Dae Seog Heo
Publication year - 2009
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm_00000196
Subject(s) - stat1 , stat3 , cancer research , head and neck squamous cell carcinoma , stat protein , janus kinase , jak stat signaling pathway , apoptosis , stat , biology , oncogene , cell growth , cell , cell cycle , signal transduction , cancer , head and neck cancer , microbiology and biotechnology , tyrosine kinase , genetics
The family of signal transducers and activators of transcription (STAT) are transcription factors. Among them, STAT1 is associated with an apoptosis pathway, while STAT3 is associated with tumorigenicity in various cancer cells. In order to investigate the primary roles of STAT1 and STAT3 in head and neck squamous cell carcinoma (HNSCC), we blocked STAT3 with two JAK inhibitors: AG490 (JAK2-STAT3 pathway inhibitor) and JAK total inhibitor. When we inhibited STAT3 with AG490, significant cell death was observed. However, in the case of JAK kinase total inhibitor, no cell growth retardation was observed. We focused on the role of STAT1 in this phenomenon. Suppression of STAT1 by si-RNA resulted in increased cell survival. Furthermore, the growth inhibitory effect of AG490 was reduced by treatment with si-RNA of STAT1. These results reveal that STAT1 is required to promote the tumor killing effect of STAT3 inhibition in HNSCC.