Ask about this productRelated genes to: CHEK1 Blocking Peptide
- Gene:
- CHEK1 NIH gene
- Name:
- checkpoint kinase 1
- Previous symbol:
- -
- Synonyms:
- CHK1
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-21
- Date modifiied:
- 2011-11-11
Related products to: CHEK1 Blocking Peptide
Related articles to: CHEK1 Blocking Peptide
- Tyrosine kinase inhibitors represent the most effective and long-lasting treatment currently available for aggressive thyroid cancers, but in some patients the response is poor or absent. Recently, we demonstrated that the response to Lenvatinib is associated with alterations in gene or protein. Aiming to find a novel therapeutic strategy for aggressive thyroid cancers, we investigated the DNA damage response pathway, where p53 plays a crucial role, and tested its inhibition through synthetic lethality or stress sensitization strategies. - Source: PubMed
Publication date: 2026/05/08
Manzo AlessandroGrassi Elisa StellariaBorghi Maria OriettaColombo CarlaPersani LucaCirello Valentina - Hepatocellular carcinoma (HCC) metastasis often threatens patient survival. However, there is still a lack of effective treatments to tackle this problem. Ruanjianhugan tablets (hepatoprotective and fibrolytic tablets), a traditional Chinese herbal compound, have demonstrated potential in repressing the progression of HCC. However, the exact active ingredients and mechanisms behind its effects are not yet fully understood. In this study, we leveraged network-pharmacology tools to screen the key bioactive constituent-calycosin (Cal)-from this compound formula and predicted it as the target for the downstream gene checkpoint kinase 1 (CHEK1) in HCC cells. Subsequent cellular thermal shift assay (CETSA) verified that Cal bound CHEK1. , CCK-8, colony-formation, Transwell and Western-blot assays showed that Cal markedly suppressed HCC-cell proliferation, colony formation, migration, invasion and epithelial-to-mesenchymal transition. In xenograft nude-mouse and tail-vein lung metastasis models, exogenous Cal bound CHEK1 and thereby inhibited HCC metastasis and tumor growth. Collectively, these results not only establish Cal as the core pharmacodynamic component of Ruanjianhugan tablets but also unveil a novel Cal-CHEK1 axis underlying anti-HCC metastasis. - Source: PubMed
Publication date: 2026/05/21
Wan PeiqiLiu ZhihongLi KaiWen ZhangNing QiuyueXiao Fang - : Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. : Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. : These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. - Source: PubMed
Publication date: 2026/04/23
Rutecki SzymonKrawiec AdriannaLeśniewska-Bocianowska AgnieszkaMatuszewska JuliaNaumowicz ErykSzubert SebastianKsiążek KrzysztofMikuła-Pietrasik Justyna - Embryonic genome activation (EGA) marks the onset of transcriptional autonomy in the developing embryo, a process that is still not well characterized in pigs. Emerging evidence suggests that chromatin remodeling events during EGA and DNA damage response (DDR) may share regulatory mechanisms. In mouse and human embryos, the double homeobox (Dux) transcription factor acts as a pioneer regulator of EGA and may also contribute to DDR. However, the role of the porcine orthologue, DUXA, in early embryogenesis is not well understood. In this study, we show that DUXA mRNA is highly expressed in porcine embryos at the EGA stage, with levels declining at post-EGA and blastocyst stages. Attenuation of DUXA mRNA did not impair blastocyst formation or lineage allocation to the inner cell mass and trophectoderm. Unexpectedly, DUXA mRNA attenuation increased total cell number in both blastocysts and embryos arrested prior to blastocoel formation. DUXA mRNA attenuation decreased mRNA levels of EGA-related (EIF1AX), cell cycle checkpoint (CHEK1), and DDR-associated genes (BRCA1), and was accompanied by increased DNA damage at late/post-EGA stages. Induced DNA damage upregulated transcripts of EGA-related (DPPA2, KDM5B, EIF2A) and DDR-associated genes (P53, RAD51) on day 4 of development. Interestingly, DNA damage induction in DUXA mRNA-attenuated embryos abrogated the impact on cell proliferation and enhanced transcript levels of checkpoint (CHEK1 and XIAP) and DDR (P53, KU-70 and KU-80) genes. These findings suggest that while DUXA is not essential for parthenogenetic blastocyst formation in pigs, it may play a regulatory role in embryonic cell proliferation, checkpoint activation, and the DNA damage response. - Source: PubMed
Publication date: 2026/05/12
Facioli Fernanda LuizaGlanzner Werner GiehlGutierrez Karinade Macedo Mariana Priottoda Silva ZigomarGuay VanessaCurrin Luke GeorgeCarrillo Herrera María ElenaBordignon Vilceu - Olaparib is registered for use in ovarian, breast, pancreatic and prostate cancers with a BRCA1/2 mutation and/or mutations in other homologous recombination deficiency (HRD) genes. HRD gene mutations are also found in other cancer types, and these cancers may also benefit from olaparib therapy. We aimed to evaluate the efficacy of olaparib in advanced cancers harboring a (likely) pathogenic germline or somatic mutation in a gene involved in homologous recombination (HR). - Source: PubMed
Publication date: 2026/05/08
Joris SDenys HCollignon JRasschaert Mde Roodenbeke D TDuhoux F PCanon J LTejpar SMebis JDecoster LAftimos PDe Grève J