ABSTRACT
The occurrence of pancreatic duct adenocarcinoma (PDAC) is closely related to the biological immunological characteristics of the hematopoietic matrix of its cancer cells.The malignant characteristics of the cancer matrix play important roles in the malignant origin of tumors,avoiding immune surveillance,promoting tumor progression and growth,and increasing drug resistance and metastasis.Understanding the important roles of hyaluronic acid,Sonic Hedgehog signaling pathway,transforming growth factor-beta,CD40,Kras pathway and microRNA in the pathogenesis and development of PDAC,can provide new strategies for clinical treatment of PDAC.
ABSTRACT
Objective To explore the correlation of E-cadherin expression and the sensitivity to EGFR-TKI molecular targeted therapy. Methods Eight kinds of cells,MCF-7,MDA-MB-231,T24,SiHa,H460,SK-HEP-1,MHCC97-H and THP-1 were treated with EGFR-TKI PD153035 and gefitinib,respectively,for 48 hours. The drug-sensitivity was detected by MTT,and the IC50 of cells were calculated. The E-cadherin protein were detected and compared. Results Followed with PD153035 and gefitinib treatment,the survival rates of MCF-7,MDA-MB-231,T24 and SiHa significantly reduced,and more E-cadherin protein expressed. However, the survival rates of the H460, SK-HEP-1, MHCC97-H, and THP-1 cells showed opposite results. Conclusion The sensitivity of epithelial cancer cells to EGFR-TKI is correlated with E-cadherin expression. E-cadherin may play a significant role on regulateing the sensitivity to EGFR-TKI molecular targeted therapy. E-cadherin is a key biomarker for recruiting appropriate patients for EGFR-TKI molecular targeted therapy.