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Moreover, the level of phospho-EGFR was increased in OS cells when exposed to gemcitabine treatment. A more profound proliferative inhibition and a higher rate of apoptosis were obtained in OS cells via inducing cell cycle arrest at G1 phase upon gemcitabine treatment combined with EGFR knockdown, as compared to gemcitabine alone. On the contrary, EGFR overexpression counteracted the growth-inhibiting and pro-apoptotic effects of gemcitabine in OS cells. The present study suggests that EGFR promotes tumor progression and contributes to g
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