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Background Lung cancer is the leading cause of cancer death worldwide. Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer. The incidence and prognosis in NSCLC demonstrates gender difference [1,2]; therefore, sex steroids and/or their receptors may play important roles during lung tumorigenesis and cancer progression. In our previous investigation, cell proliferation, migration, invasion, and tumor formation were inhibited by shRNA interference of androgen receptor (AR) in non-small cell lung cancer (NSCLC) cells lines. The expressions of cyclin D1 also decreased to less than 50% after AR knockdown. However, the roles of androgen receptor in treatment of NSCLC are still controversial.

Targeting androgen receptor as a new potential therapeutic approach to battle tobacco carcinogens-induced non-small cell lung cancer