Ask about this productRelated genes to: CDK6 antibody
- Gene:
- CDK6 NIH gene
- Name:
- cyclin dependent kinase 6
- Previous symbol:
- -
- Synonyms:
- PLSTIRE
- Chromosome:
- 7q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-14
- Date modifiied:
- 2019-04-23
Related products to: CDK6 antibody
Related articles to: CDK6 antibody
- Cyclin-dependent kinase 4/6 (CDK4/6) inhibitors such as palbociclib have improved the treatment of hormone receptor-positive, luminal A breast cancer; however, therapeutic resistance remains a major challenge. Wild-type p53-induced phosphatase 1 (Wip1) is a negative regulator of the p53 pathway and is often over-expressed in luminal breast cancers. This study aimed to determine whether Wip1 inhibition enhances the anti-proliferative and pro-apoptotic effects of the CDK4/6 inhibitor palbociclib in luminal A breast cancer cells and to elucidate the underlying cell cycle-related mechanisms. MCF-7 cells were treated with palbociclib and Wip1 inhibitor GSK2830371, alone or in combination. Cell viability was assessed using the WST-1 assay, cell cycle distribution was analysed by flow cytometry, and apoptosis was evaluated using Annexin V/7-aminoactinomycin D staining. Expression of cell cycle regulators (CDK2, CDK4, CDK6, cyclin D1/D3, Rb, phospho-Rb) and p53-related proteins (p53, phospho-p53 Ser15, p21, p27) was determined by Western blot analysis. The combined treatment produced a concentration-dependent reduction in cell viability and a marked increase in both early and late apoptotic populations compared with monotherapies. While palbociclib alone induced G1 arrest, co-treatment with GSK2830371 shifted cells toward G2 accumulation. This was accompanied by enhanced phosphorylation of p53, up-regulation of p21 and p27, and dephosphorylation of Rb, indicating dual checkpoint engagement. These findings demonstrate that Wip1 inhibition augments palbociclib-mediated cell cycle arrest and apoptosis through modulation of the p53-Rb axis. The dual blockade of Wip1 and CDK4/6 may represent a promising therapeutic strategy for p53-proficient luminal A breast cancer. - Source: PubMed
Çolak GökhanKaygusuz NazllcanMeydan NezihOktay EsinKılıc Eren Mehtap - The overactivated CDK6/Cyclin D3 complex is considered to be associated with poor prognosis in patients with NSCLC, thus developing CDK6/Cyclin D3 inhibitors is expected to provide new options for NSCLC patients. This study successfully utilized a mixed virtual screening workflow based on artificial intelligence, pharmacophores, and docking to rapidly identify multiple CDK6/Cyclin D3 inhibitors from a compound library consisting of 12,563 compounds, achieving a hit rate of over 40% (2 out of 5 selected candidate compounds). Among these, compound 2 exhibited the most potent CDK6/Cyclin D3 inhibitory activity, with an IC value of 38.6 nM, comparable to CDK6 inhibitors in clinical trial phases. In vitro antitumor activity indicated that compound 2 has strong proliferation-inhibitory activity against NSCLC, with IC values below 78 nM for two NSCLC cell lines, showing promise for further exploration. Kinetic simulation results revealed that compound 2 binds to the ATP-binding pocket of CDK6, stabilizing its conformation through hydrogen bond interaction with Val101 and ionic interaction with Asp104, providing new insights for the development of subsequent CDK6 inhibitors. - Source: PubMed
Publication date: 2026/05/15
Xu YanaWang ZhehanYang TianhuaWang HanHou LepingWang XiangYang GaoyiLuo Ying - A working group of cIMPACT-NOW evaluated the literature on IDH-mutant gliomas for opportunities to improve pathology-based risk stratification and grading, especially at the interface of CNS WHO grade 2 and 3, since therapeutic decisions depend on risk assessment for clinical management. The group also evaluated newly described IDH-mutant glioma subgroups and considered multidisciplinary aspects of therapeutic decision-making. PDGFRA amplification was associated with highly aggressive clinical behavior of IDH-mutant astrocytomas, consistent with CNS WHO grade 4. Other genetic alterations associated with intermediate risk and most consistent with CNS WHO grade 3 included PIK3 mutations, EGFR amplification, MYCN amplification and specific RB pathway alterations, including CDK4, CDK6 and CCND2 amplification, RB1 homozygous deletion or mutation, and mutation of CDKN2A. DNA methylation signatures of G-CIMP-low or A_IDH_HG were consistent with CNS WHO grade 3 or 4, depending upon other grading criteria. We suggest a mitotic count of ≥ 3 per 2.4 mm2 could be considered as a CNS WHO grade 3 criterion. Our review did not uncover features to improve grading of oligodendroglioma, IDH-mutant and 1p/19q-codeleted, although CNS WHO grade 3 tumors with elevated mitotic rates, yet lacking necrosis, microvascular proliferation, CDKN2A/B homozygous deletion and MRI contrast enhancement, may be associated with extended survival. Implementing evidence-based criteria for risk stratification and grading will improve guidance for clinical decision-making. - Source: PubMed
Publication date: 2026/05/18
Brat Daniel JAldape KennethFrench Pim JLouis David NNasrallah MacLean PReifenberger GuidoReuss David ETouat Mehdivan den Bent Martin JWesseling PieterFigarella-Branger Dominique - To evaluate the safety and efficacy of CDK4/6 inhibitors in combination with hormone therapy, and to investigate potential predictive markers of treatment in metastatic breast cancer (MBC). - Source: PubMed
Demirel NadideYildiz BulentDemir Metin - Transmembrane Emp24 Domain Containing 2 (TMED2) is involved in various cancers, but its role in diffuse large B-cell lymphoma (DLBCL) remains unclear. This study investigated TMED2's expression, biological functions, and underlying mechanisms in DLBCL. - Source: PubMed
Publication date: 2026/05/01
Qian WeiYang Mingzhen