Objective:Previous reported have demonstrated that an intricate link between epithelial-mesenchymal transition(EMT) and anticancer drug resistance in cell culture and animal model. The aim of this study is to further investigate the relationship between chemoresistance and EMT in non-small cell lung cancer(NSCLC) through observing the expression status of EMT markers and resistance protein in histological level. Methods: The resistance protein, excision repair cross-complementing 1(ERCCl) and EMT markers, including E-cadherin and vimentin, were detected by immunohistochemistry in 100 cases of NSCLC, half of that were treated with pre-operative neoadjuvant chemotherapy(neoadjuvant chemotherapy group), and the other underwent surgery alone(simple surgery group). Results: There were significant positive correlations between the expression of ERCCl and vimentin in neoadjuvant chemotherapy group(r =0.471,P = 0.01) and simple surgery group( r = 0.380,P = 0.01), and significant negative correlations between the ERCCl and E-cadherin in neoadjuvant chemotherapy group(r =-0.401,P = 0.01) and simple surgery group(r =-0.295,P = 0.03.In neoadjuvant chemotherapy group, EMT status(p = 0.04) and drug resistance(p = 0.03) were more apparent than simple surgery group. The expression levels of ERCCl, vimentin and E-cadherin were all related to differentiated degree and lymph node metastasis in both groups(P < 0.05). Conclusion: This study indicated that chemoresistance is correlated with the occurrence of EMT in NSCLC at tissue level, suggesting that selective targeting of EMT-phenotypic cells for declining chemoresistance may be a plausible therapeutic strategy. Objective: Previous reported have previously demonstrated that an intricate link between epithelial-mesenchymal transition (EMT) and anticancer drug resistance in cell culture and animal model. The aim of this study is to further investigate the relationship between chemoresistance and EMT in non-small cell lung Methods: The resistance protein, excision repair cross-complementing 1 (ERCCl) and EMT markers, including E-cadherin and vimentin, were detected by immunohistochemistry in 100 cases of NSCLC, half of that were treated with pre-operative neoadjuvant chemotherapy group (neoadjuvant chemotherapy group), and the other underwent surgery alone (simple surgery group). Results: There were significant positive correlations between the expression of ERCCl and vimentin in neoadjuvant chemotherapy group (r = 0.471, P = 0.01) and simple surgery group (r = 0.380, P = 0.01) lations between the ERCCl and E-cadherin in neoadjuvant chemotherapy group (r = -0.401, P = 0.01) and simple surgery group (r = -0.295, P = 0.03.In neoadjuvant chemotherapy group, EMT status resistance (p = 0.03) were more apparent than simple surgery group. The expression levels of ERCCl, vimentin and E-cadherin were all related to differentiated degree and lymph node metastasis in both groups (P <0.05). Conclusion: This study indicated that that chemoresistance is correlated with the occurrence of EMT in NSCLC at tissue level, suggesting that selective targeting of EMT-phenotypic cells for declining chemoresistance may be a plausible therapeutic strategy.