Akt isoforms differentially provide for chemoresistance in prostate cancer.

ABSTRACT:

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 chemoresistant. We 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 functioning. Here, we characterized Akt isoform expressions in primary and metastatic prostate cancers, as well as their individual contributions to chemoresistance.

Methods

Akt isoforms and E-cadherin were manipulated with drugs, knocke

SUBMITTER: Ma B 

PROVIDER: S-EPMC9196054 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature