Abstract
Lung squamous cell carcinoma (LSCC) is a common histological lung cancer subtype, but unlike lung adenocarcinoma, limited therapeutic options are available for treatment. Curcumin, a natural compound, may have anticancer effects in various cancer cells, but how it may be used to treat LSCC has not been well studied. Here, we applied curcumin to a human NCI-H292 LSCC cell line to test anticancer effects and explored underlying potential mechanisms of action. Curcumin treatment inhibited NCI-H292 cell growth and increased FOXA2 expression in a time-dependent manner. FOXA2 expression was decreased in LSCC tissues compared with adjacent normal tissues and knockdown of FOXA2 increased NCI-H292 cells proliferation. Inhibition of cell proliferation by curcumin was attenuated by FOXA2 knockdown. Moreover inhibition of STAT3 pathways by curcumin increased FOXA2 expression in NCI-H292 cells whereas a STAT3 activator (IL-6) significantly inhibited curcumin-induced FOXA2 expression. Also, SOCS1 and SOCS3, negative regulators of STAT3 activity, were upregulated by curcumin treatment. Thus, curcumin inhibited human NCI-H292 cells growth by increasing FOXA2 expression via regulation of STAT3 signaling pathways.
Highlights
Lung cancer, a highly malignant tumor associated with mortality, can occur as small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC) (Malanga et al, 2008; Bersaas et al, 2016)
Our data agree with previous studies that curcumin inhibited cell proliferation of Lung squamous cell carcinoma (LSCC) NCI-H292 cells in a time- and dose-dependent manner (Amin et al, 2015; Haque et al, 2015)
NCI-H292 cells growth might be associated with increasing FOXA2 expression, suggesting that FOXA2 is a novel target of curcumin
Summary
A highly malignant tumor associated with mortality, can occur as small cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC) (Malanga et al, 2008; Bersaas et al, 2016). Lung squamous cell carcinoma (LSCC), formerly the most common histologic subtype of NSCLC, is characterized by a poor therapeutic response, a high relapse rate, and poor prognosis (Justilien et al, 2014). Unlike lung adenocarcinoma, limited therapeutic options are available for advanced-stage LSCC, new and better targets or drugs are needed. Studies suggest that FOXA2 may be a suppressor of tumor metastasis in human lung cancers (Tang et al, 2011). FOXA2 regulates the expression of genes critical to lung morphogenesis, and loss of FOXA2 expression is frequent in lung cancer cell lines (Khoor et al, 2004). Squamous cell carcinomas uniformly lack FOXA2 staining (Khoor et al, 2004).
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