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GIT1 Regulates Lung Cancer Metastasis through Modulating Rac1/Cdc42 Activity and Acts as an Independent Prognostic Factor in Human Non‐Small Cell Lung Cancer.
Author(s) -
Chang JengShou,
Hua KuoTai,
Kuo MinLiang,
Hsiao Michael
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.54.7
Subject(s) - rac1 , lung cancer , metastasis , cdc42 , cancer , cancer research , medicine , tissue microarray , oncology , biology , cell , signal transduction , biochemistry , genetics
Lung cancer is the leading cause of cancer‐related deaths worldwide and the prognosis of NSCLC remains poor. Identification of novel prognostic markers and therapeutic targets are urgently needed. Here we identified G‐protein‐coupled receptor‐kinase interacting protein 1 (GIT1) gene from 5,000 High‐throughput antibodies library screening using tissue microarray (TMA) after comparing protein expression differences of five major human cancer primary tumors and normal adjacent tissues. The results were further confirmed by online microarray database analysis to show GIT1 as a top‐ranked prognosis predictor in NSCLC. Further multivariate analysis showed high GIT1 expression is significantly associated with poor prognoses in DFS and OS. Mechanistically, we identified GIT1 as a master regulator of Rac1/Cdc42 axis in regulating lung cancer cell motility in vitro and in vivo. GIT1 can promote lung cancer cell metastasis by altering Rac1/Cdc42 activity. Taken together, our results showed GIT1 overexpression is associated with poor prognosis and can be considered an early prognosis marker in patients with NSCLC.