H2AX (H2A.X Variant Histone)

Furthermore, the combination treatment induced G2/M phase cell cycle arrest by modulating the ATM-Chk2 signaling pathway. This study demonstrates that the combination of lenvatinib and BP represents a promising therapeutic strategy for CRC by enhancing apoptosis and cell cycle arrest through ROS-mediated DNA damage.

In addition, 15b displayed strong anti-inflammatory activity in LPS-stimulated BV-2 microglia, reducing mRNA and protein levels of IL-1β, IL-6, TNF-α, iNOS, COX-2, and NLRP3, indicating multi-target inhibition of neuroinflammation. In summary, compound 15b exhibits dual anticancer and anti-inflammatory activities by inducing DNA damage, activating apoptotic pathways in tumor cells, and suppressing key pro-inflammatory mediators, highlighting its potential as a lead compound for the development of anticancer drugs with anti-depressive properties.

The thread effect in HT can be harnessed for SFRT, avoiding traditional mitigation strategies. The optimized HT-SFRT scheme (32 Gy/4 F) offers equivalent tumor control, shorter treatment duration, and acceptable normal tissue toxicity, providing a promising alternative for gynecological cancer radiotherapy. Prospective clinical trials are warranted to validate these findings.

The compound demonstrates significant cytotoxic efficacy against HeLa cervical cancer cells, exhibiting a substantially reduced IC₅₀ value and an elevated selectivity index relative to Doxorubicin and Ferrocene...Subsequent assessments related to apoptosis revealed distinct nuclear condensation and fragmentation through DAPI staining, along with notable DNA double-strand break production indicated by γ-H2AX expression. Furthermore, 3D multicellular spheroid experiments validated the penetrating ability and prolonged anticancer effectiveness of FBP in a tumor-mimicking environment.

Upregulation of γ-H2AX, a key DNA damage marker, was confirmed by both immunofluorescence and Western blot analysis, indicating that the antitumor activity of 15 h is closely associated with the induction of DNA damage. In conclusion, compound 15 h effectively suppresses tumor cell proliferation and induces apoptosis through ROS-mediated DNA damage, demonstrating promising potential for development as a novel DNA-targeting anticancer agent.

In vitro experiments demonstrated that 6-hydroxyluteolin and isorhamnetin significantly inhibited cell proliferation, upregulated γ-H2AX expression levels, induced cell cycle arrest, and ultimately induced apoptosis. We found that Evodia rutaecarpa exerts anti-esophageal cancer effects through multiple components, targets, and pathways, thereby providing a theoretical basis for the potential application of Evodia rutaecarpa in the treatment of esophageal cancer.

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.