siRNA-Based Approaches for Castration-Resistant Prostate Cancer Therapy Targeting the Androgen Receptor Signaling Pathway

Abstract

Androgen deprivation therapy is a common treatment method for metastatic prostate cancer through lowering androgen levels; however, this therapy frequently leads to the development of castration-resistant prostate cancer (CRPC). This is attributed to the activation of the androgen receptor (AR) signaling pathway. Current treatments targeting AR are often ineffective mostly due to AR gene overexpression and mutations, as well as the presence of splice variants that accelerate CRPC progression. Thus there is a critical need for more specific medication to treat CRPC. Small interfering RNAs have shown great potential as a targeted therapy. This review discusses prostate cancer progression and the role of AR signaling in CRPC, and proposes siRNA-based targeted therapy as a promising strategy for CRPC.

Keywords::

• ADT
• androgen receptor
• CRPC
• CSPC
• prostate cancer
• siRNA

Supplementary data

To view the supplementary data that accompany this paper please visit the journal website at: www.tandfonline.com/doi/suppl/10.2217/fon-2023-0227

Author contributions

D Papukashvili and X Lu: conceptualization. Y Yu, R Ren, D Papukashvili and W Bai: literature search. N Rcheulishvili and D Papukashvili: writing the original draft, revision. S Feng, H Zhang and Y Xi: visualization. X Lu and N Xing: supervision. All authors have read and agreed to the published version of the manuscript.

Financial disclosure

This work was supported by the National Natural Science Foundation of China (grant Nos. 82002820, 82172659 and 82072740). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Competing interests disclosure

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China (grant Nos. 82002820, 82172659 and 82072740). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.