RACK1 induces chemotherapy resistance in esophageal carcinoma by upregulating the PI3K/AKT pathway and Bcl-2 expression

Introduction: Accumulating evidence in indicatesdicates that RACK1 is ntvolved in the progression of tumors. We aimed to evaluate the function of RACK1 in esophageal squamous cell carcinoma (I SE and its role in the mechanism of chemotherapy resistance. Materials and methods: Transfected ESCC cell lines with plasmids expressed shRACK1 or open reading frame (OR F) targeting RACK1 and established stable cell lines. We then examined the effects of RACK1 ON on cell proliferation and chemotherapy resistance in ESCC cell lines, and the expression of AKT, pAKT, ERK1/2, Bcl-2, and Bim Was introduced to thriller detect the association between RACK1 and chemotherapy resistance. Results: The proliferation ability of ESCC cells was improved in the overexpression RACK1 groups (P<0.001) and decreased in the transfected shRACK1 groups (P<0.001) compared with the control ones. Meanwhile, upregulation of RACK1 significantly suppressed cisplatin-induced apoptosis in Eca 109 and EC'9706 cells, while downregulation of RACK1 promoted the sensitivity compared to the control group (Eca 1 09: P<0.00I for sh RACK1, 1<0.01 for shNC, and P<0.001 for overexpression group; EC9706: P<0.00I for sh RACK1, P<0.00I for sliNC, and 1'<0.05 for overexpression group). Furthermore, we found that RACK1 could activate the P13K/AKT pathway and increase the expression level of I3c1-2 in ESCC, which leads to the enhancement of chemoresistance in ESCC. Conclusion: RACK1 promotes proli aeration and chemotherapy resistance in 13SCC by activating the PI3K/AKT pathway and upregulating the Bel -2 expression.