H2AX (H2A.X Variant Histone)

PTEN enhances the radiosensitivity of melanoma by inhibiting the DNA-PKcs signal, weakening NHEJ repair, and delaying cell-cycle recovery. PTEN can serve as a biomarker for radiotherapy response prediction and a target for sensitization intervention, providing an experimental basis for precise radiotherapy strategies for melanoma.

Senolytic plus senogenic combinations demonstrate robust preclinical efficacy in reducing tumor growth and senescent burden while promoting apoptosis across diverse in vivo models. These findings highlight senotherapy as a promising adjunct to conventional senescence-inducing anticancer therapies and underscore the need for standardized in vivo methodologies and translational studies to guide clinical application. This review protocol was prospectively registered on PROSPERO (registration number: CRD420251161998).

Collectively, these findings highlight RPGRIP1L as a key genomic instability-maintaining gene in human breast cancer, offering critical insights into the molecular mechanisms underlying disease progression. Furthermore, targeting RPGRIP1L may represent a promising therapeutic strategy for breast cancer.

Overexpression of NFE2L1-DT or ALKBH5, or silencing Cx43, attenuated the protective effects of IRF1 silencing against radiation-induced damage. These findings indicate that radiation-induced IRF1 upregulation leads to endothelial injury by promoting pyroptosis through the NFE2L1-DT/ALKBH5/Cx43 axis.

Mechanistically, PIBF1-WT resisted cisplatin-induced DNA damage, significantly down-regulated the expression of γ-H2AX, and affected DNA damage repair, thus exerting a cancer inhibitory function...Furthermore, this family's polygenic risk factors for cancer are analyzed, and there is speculation about potential synergistic effects between PIBF1 and DNA damage repair genes like BRCA2 and RAD51D. In conclusion, PIBF1 regulates the cell cycle and DNA damage repair, PIBF1(p.R405Q) increases susceptibility to cancer, multiple DNA damage repair gene mutations may synergistically promote cancer progression in this cancer family lineage, and PIBF1(p.R405Q) may be one of the polygenic risk factors for familial hereditary cancer syndromes.

Functional analysis of target genes, CCND1 as a key gene through which miR-20b enhanced radiosensitivity in HPV+ HNSCC. In this study, our results suggest that M1 exos, enriched with miR-20b, regulate the DNA damage repair pathway in tumor cells by targeting CCND1, enhancing the radiosensitivity of HPV+ HNSCC.

Collectively, the present study establishes the potential of Houttuynia cordata-derived exosome-like nanovesicles as a natural therapeutic platform against TNBC, with macrophage membrane coating further augmenting their efficacy through biomimetic targeting. MCELNs may represent a promising drug delivery strategy for enhancing treatment efficacy while minimizing systemic toxicity in breast cancer therapy.

γ-H2AX overexpression in PDAC tissue is an independent negative prognostic factor. In recurrent cases, high γ-H2AX expression suggests better OS and treatment response with mFOLFIRINOX, indicating its potential as a chemosensitivity marker for personalized therapy in PDAC recurrence.

This combination significantly increased apoptosis, measured by flow cytometry, and increased levels of γ-H2AX protein and 8-oxo-2'-deoxyguanosine.Diosgenin significantly augmented methotrexate-mediated apoptosis in Saos-2 cells through enhanced DNA damage mechanisms. These findings suggest that diosgenin could serve as a promising adjuvant therapeutic agent to improve the efficacy of current methotrexate-based chemotherapy regimens in osteosarcoma treatment, potentially reducing required drug doses and minimizing associated toxicity while maintaining therapeutic effectiveness.

Collectively, our study demonstrates that MOF promotes DNA damage repair and enhances CR in lung cancer cells via H4K16ac-mediated WSTF acetylation. These findings provide valuable insights for overcoming chemoresistance and improving patient outcomes.

In conclusion, MCPT exerts antimelanoma effects by inhibiting proliferation, inducing cell cycle arrest, DNA damage, and apoptosis. Importantly, these effects are critically mediated through the downregulation of PAF15.

GDF15 is implicated in the progression of thyroid cancer and potentially modulates cellular senescence through a p53-dependent mechanism, underscoring its dual functionality as both a pro-tumorigenic driver and a senescence regulator. These findings establish the potential of GDF15 as a therapeutic target and prognostic biomarker in thyroid cancer, providing novel insights developing senescence-centered therapeutic strategies.