Abstract
Organisms evolved into different species to adapt to the environment according to the laws of Darwinian evolution. In a single life, prostate cancer cells can also evolve into tumor stem cells to adapt to the microenvironment, such as different chemotherapeutic drugs. These cancer cells become an unrestricted growth group relatively independent of the individual. The present review attempts to establish evidence that prostate cancer cells may survive by hormonotherapy and chemotherapy by gene amplification, mutation, and alternative splicing. Simultaneously, novel treatment strategies have been cited and evaluated, avoiding the resistance mechanisms.
Highlights
In Europe and the USA, prostate cancer (PCa) is one of the most common malignant tumors and the second leading cause of cancer-related deaths in men
The androgen receptor (AR) is a key driver molecule leading to the occurrence and progression of PCa, even in the stage of castration-resistant PCa (CRPC)
It is encoded by eight exons and has four structural domains: the N-terminal transcriptional activation domain, the DNA-binding domain (DBD), a hinge region, and the C-terminal ligand-binding domain (LBD)
Summary
In Europe and the USA, prostate cancer (PCa) is one of the most common malignant tumors and the second leading cause of cancer-related deaths in men. AR is a key driver molecule to take part in PCa development and progression, response to initial ADT, and subsequent resistance to chemotherapeutics. These malignant cells undergo several adaptive changes to ensure persistent androgen signaling. A correlation between elevated expression of full-length AR or AR copy number gains resistant to second-generation antiandrogens has been documented [5] This could be explained by an adaptive pharmacokinetic change, in which, the androgen is unable to achieve sufficient concentrations within the tumor, and the increased intratumoral steroidogenesis overcomes the inhibitory effects of antiandrogens [6]. Constant expression of AR-v567es in the benign prostate tissues may induce epithelial hyperplasia and invasive adenocarcinoma [10]
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