Ask about this productRelated genes to: p16INK4a antibody
- Gene:
- CDKN2A NIH gene
- Name:
- cyclin dependent kinase inhibitor 2A
- Previous symbol:
- CDKN2, MLM
- Synonyms:
- CDK4I, p16, INK4a, MTS1, CMM2, ARF, p19, p14, INK4, p16INK4a, p19Arf, p14ARF
- Chromosome:
- 9p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-19
- Date modifiied:
- 2019-04-23
Related products to: p16INK4a antibody
Related articles to: p16INK4a antibody
- Malignant rhabdoid tumors (MRT) are highly aggressive pediatric malignancies driven by SMARCB1 loss and consequent epigenetic dysregulation, with dismal survival rates underscoring the need for novel therapies. Given the central role of chromatin modifiers in MRT pathogenesis, we investigated a novel combinatorial epigenetic approach simultaneously targeting histone deacetylases (HDACs) and bromodomain and extraterminal (BET) family proteins. Using a focused epigenetic compound screen across multiple MRT cell lines, we identified that the HDAC inhibitor panobinostat (LBH589) and the BET inhibitor birabresib (OTX015) act synergistically to inhibit cell proliferation, with combination index (CI) values consistently <1. Transcriptomic profiling revealed that this synergy is underpinned by a profound downregulation of cell cycle genes, leading to G1/S phase arrest. Mechanistically, the combination therapy cooperatively restores the expression of the cyclin-dependent kinase inhibitors p21 and p16. This restoration inhibits cyclin D1-CDK4/6 kinase activity, reduces retinoblastoma protein (Rb) phosphorylation, and consequently represses the E2F1 transcriptional program and its key targets, including cyclin A2 and cyclin B1. In vivo, this dual-epigenetic targeting significantly attenuated tumor growth in MRT xenograft models, outperforming either monotherapy, and was associated with suppressed proliferation and E2F1 signaling. Our findings unveil a novel synergistic strategy that pharmacologically recapitulates a core SMARCB1-mediated tumor-suppressive circuit, nominating combined HDAC and BET inhibition as a promising therapeutic avenue for MRT. - Source: PubMed
Publication date: 2026/06/22
Zhu LingyanLi YuanyuanWen YaxianWen JinxuanZhang JunzhuMin LingzhaoLi ChangshengPeng QiWang LishaLi AnqiLiu ZebingWang Xiaoqiang - Intervertebral disc degeneration (IDD) is frequently associated with chronic low back pain (LBP), which contributes significantly to disability, psychological distress, and reduced work capacity. Mesenchymal stromal cell (MSC)-based treatments may offer a promising, less invasive alternative to conventional treatments for IDD. The MSC secretome has shown regenerative potential through paracrine and anti-inflammatory mechanisms. In this study, we investigated the effects of the secretome isolated from interleukin-1β (IL-1β)-preconditioned bone marrow-derived MSCs (BM-MSCs) on human nucleus pulposus cells (hNPCs) adopting a 3D in vitro culture model. - Source: PubMed
Publication date: 2026/06/20
Tilotta VeronicaVadalà GianlucaAmbrosio LucaDi Giacomo GiuseppinaCicione ClaudiaRusso FabrizioPapalia RoccoDenaro Vincenzo - Mesenchymal stromal cells (MSCs) possess therapeutic potential largely reliant on intact mitochondrial function to maintain reparative function. However, obesity compromises MSC metabolism and reparative capacity. MOTS-c, a mitochondria-derived peptide, is known to regulate cellular metabolism, but its role in human MSC biology remains unclear. We hypothesized that restoring MOTS-c signaling rescues the impaired functionality of adipose-derived MSCs from individuals with obesity. - Source: PubMed
Publication date: 2026/06/22
Xing LiLu BoZhu XiangyangAl Saeedi MinaLerman AmirEirin AlfonsoCohen PinchasLerman Lilach O - Disulfidptosis and cuproptosis are recently identified forms of regulated cell death whose component genes may harbor prognostic information in oral squamous cell carcinoma (OSCC). However, no validated multi-gene prognostic signature derived from these pathways has been established. - Source: PubMed
Publication date: 2026/06/19
Yao YaoLi XiaoshanPang ZiyanKang WenmingGong LiqiangZhou QiMao Chen - Digestive system cancers (DSCs) remain among the most prevalent and lethal malignancies worldwide, accounting for more than a quarter of cancer diagnoses and a third of cancer deaths. Advances in next-generation sequencing (NGS) have accelerated discovery of genetic, epigenetic, and transcriptomic alterations, yet an integrated overview across DSCs is lacking. This scoping review synthesized 57 studies published between 2013 and 2025 from PubMed, Scopus, and Web of Science. Colorectal and gastric cancers were most frequently represented, while oesophageal, pancreatic, and rare subtypes such as gallbladder and ampullary cancers were under-studied. Recurrent alterations in TP53, KRAS, PIK3CA, and CDKN2A were identified, alongside mismatch repair deficiency and microsatellite instability in colorectal and gastric cancers. Emerging evidence from recently published studies further highlights the contribution of germline alterations and increased molecular heterogeneity in selected DSC subtypes. Epigenetic dysregulation and recent applications of single-cell and spatial transcriptomics highlighted tumour heterogeneity. Despite progress, evidence remains uneven across cancer types, with limited exploration of germline variants beyond colorectal, pancreatic, and select liver cancers. - Source: PubMed
Publication date: 2026/06/19
Tan Shirin HuiSubramaniam SivasangariLai Wei HongRazali FarahTiong Lee LenVoon Pei JyeSim Edmund Ui-Hang