Keywords
GAS5
Prostate cancer
Radiosensitivity
Molecular mechanism
ceRNA
DNA damage repair
Submitted : 2026-06-07
Accepted : 2026-06-22
Published : 2026-07-07
Abstract
Prostate cancer is a prevalent malignant tumor in the male urogenital system. Radiotherapy, which uses high-energy radiation to kill cancer cells, serves as a cornerstone for local advanced and postoperative adjuvant treatment, yet tumor radioresistance, when cancer cells survive and adapt to radiation, significantly limits therapeutic efficacy. Long non-coding RNA (lncRNA) GAS5, a critical tumor-suppressive transcript, is commonly under expressed in prostate cancer and positively regulates radiosensitivity (the tendency of cells to be destroyed by radiation) through multiple mechanisms, including competing endogenous RNA (ceRNA, a process where RNAs regulate each other’s expression by competing for shared microRNAs) regulation, DNA damage repair, cell cycle arrest, induction of apoptosis (programmed cell death), and interactions with signaling pathways. This review systematically summarizes the structural and functional characteristics of GAS5, its expression patterns in prostate cancer, and elucidates the molecular mechanisms underlying its regulation of radiosensitivity. Additionally, it explores clinical application prospects and existing challenges, providing theoretical evidence and novel insights for enhancing precision radiotherapy in prostate cancer.
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