Table 2.

A summary of the improvements in radiotherapy that have been accomplished through targeting cell cycle regulatory molecules.

Target	Phase	Molecular Mechanism
miR-106b [53]	G2/M arrest	miR-106b can inhibit the proliferation of the PCa LNCaP cells by activating P21-mediated cell cycle arrest.
The receptor of Exendin-4, namely, GLP-1R [54]	G2/M arrest	Exendin-4 promotes AMPK phosphorylation and activates downstream signaling pathways, while also inhibiting the expression of mTOR, cyclinB, and p34.
miR-449a [55]	Cdc25A, Cdc2/CyclinB	Induction of G2/M arrest.
CD105 [56]	G2/M arrest	CD105 has been shown to promote radiotherapy resistance in PCa by depleting intracellular ATP and upregulating SIRT1, which activates the BMP and TGF-β/Smad pathways. However, targeting CD105 with the TRC105 antibody has been demonstrated to enhance radiosensitivity.
Resveratrol [57]	G1/S arrest	Resveratrol has been shown to inhibit the phosphorylation of PI3K/Akt, which is an important cell survival signaling pathway in PCa 22Rv1 and PC-3 cells following radiation treatment. Additionally, resveratrol induces the phosphorylation of AMPK and promotes cell cycle arrest in a P21-dependent manner.
GnRHR [58]	G2/M arrest	Redistribution of GnRHR expression using IN3 repositioned it on the membrane surface of PC-3 cells, promoting their radiosensitivity in the recoverable phase, while IN3 had a pro-apoptotic effect.
RPS6KB1 [59]	cyclinD1, Cdc25C, G2/M arrest	The expression of ChK1, p-Cdc25C, and cyclinD1 in PCa PC-3 cells can be downregulated after RPS6KB1 is inhibited by Nexrutine. When RPS6KB1 is inhibited, and the process of NHEJ is also inhibited.
miR-16-5p [60]	Cyclin D1/Cyclin E1/pRb/E2F1	MiR-16-5p has been shown to downregulate cyclinD1 and E1 expression in PCa LNCaP cells by directly binding with their 3′UTR region, leading to cell cycle arrest at the G0/G1 phase.