Despite breakthroughs in our understanding of lung cancer risk, development, immunologic control, and therapy choices, it remains one of the leading causes of cancer mortality. This study aimed to investigate the role of TRIM34 upon treatment of Interferon Gamma (IFN-γ) in Non-Small Cell Lung Cancer (NSCLC). NCI-H23 cells were exposed to IFN-γ in a dose- and time-dependent manner to understand TRIM34 expression and its role as a co-regulator of treatment. The regulatory role of TRIM34 on IFN-γ exposure was studied by qRT-PCR, Western blot analysis, immunocytochemistry, apoptosis assay and scratch assay. On exposure to IFN-γ, TRIM34 expression at transcript and protein level was significantly upregulated. With its upregulation, NCI-H23 underwent apoptosis and its rate of proliferation was impeded. Our results suggest that induction of TRIM34 by IFN-γ treatment may lead to an anti-tumor inflammatory response, resulting in NSCLC regression via apoptosis.
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http://dx.doi.org/10.1002/jbt.70072 | DOI Listing |
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