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akt isoforms differentially provide for chemoresistance in prostate cancer

Cancer Biology & Medicine 2022年第5期19卷 635-650页

作者： Bo Ma Hanshuang Shao Xia Jiang Zhou Wang Chuanyue(Cary)Wu Diana Whaley Alan Wells Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy Cancer InstituteXuzhou Medical UniversityXuzhou 221002China Department of Pathology University of PittsburghPittsburghPA 15261USA Pittsburgh VA Healthcare System PittsburghPA 15213USA Department of Biomedical Informatics University of PittsburghPittsburghPA 15261USA Department of Urology University of PittsburghPittsburghPA 15261USA Department of Pharmacology and Chemical Biology University of PittsburghPittsburghPA 15261USA UPMC Hillman Cancer Center PittsburghPA 15232USA

Objective:Early prostate cancer micrometastatic foci undergo a mesenchymal to epithelial reverting transition,not only aiding seeding and colonization,but also rendering the tumor cells generally *** previously found that upregulated E-cadherin in the epithelial micrometastases activated canonical survival pathways,including PI3K-akt,that protected the tumor cells from death;however,the extent of protection from blocking the pathway in its entirety was modest,because different isoforms may have alternately affected cell ***,we characterized akt isoform expressions in primary and metastatic prostate cancers,as well as their individual contributions to ***:akt isoforms and E-cadherin were manipulated with drugs,knocked down,and over *** cell killing was determined in vitro and in *** survival was calculated from patient records and ***:Pan-akt inhibition sensitized tumor cells to chemotherapy,and specific blockade of akt1 or/and akt2 caused cells to be more *** of akt3 induced apoptosis.A low dose of akt1 or akt2 inhibitor enabled standard chemotherapies to significantly eradicate metastatic prostate tumors in a mouse model,acting as *** human specimens,we found akt1 and akt2 positively correlated,whereas akt3 inversely correlated,with the overall survival of prostate cancer ***1high/akt2high/akt3low tumors had the worst ***:E-cadherin-induced activation of akt1/2 isoforms was the essential mechanism of chemoresistance,whereas akt3 made cells more *** findings emphasized the need to target akt1/2,rather than pan-akt,as a rational therapeutic approach.

关键词： Chemoresistance adjuvant therapy metastasis dormancy akt isoforms

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