Ask about this productRelated genes to: TP63 protein
- Gene:
- TP63 NIH gene
- Name:
- tumor protein p63
- Previous symbol:
- TP73L, TP53L, TP53CP
- Synonyms:
- p51, SHFM4, EEC3, p63, p73L, OFC8, KET, p73H, NBP, p53CP
- Chromosome:
- 3q28
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-18
- Date modifiied:
- 2019-04-23
Related products to: TP63 protein
Related articles to: TP63 protein
- Glioblastoma (GBM) almost inevitably recurs within 6-12 months after standard temozolomide-radiotherapy (TMZ-RT) treatment, frequently transitioning to aggressive mesenchymal (MES) states through non-genomic transcriptional reprogramming. Mutations in p53/TP53 are frequent in recurrent GBM, disabling its tumor suppressor transcriptional activity. In contrast, the related p53 family member, TP63, is rarely mutated in cancers and has been linked with MES maintenance, stemness, and therapy resistance. However, TP63 exhibits context-dependent tumor-suppressive or oncogenic roles, and its relevance to GBM recurrence remains unclear. - Source: PubMed
Publication date: 2026/05/12
Martell EmmaKuzmychova HelgiGrewal AkaljotChawla UjalaJain CharulVenugopal ChitraAnderson Christopher MSingh Sheila KSharif Tanveer - Adenoid cystic carcinoma (ACC) demonstrates marked clinical heterogeneity that is inadequately explained by conventional histopathologic and staging systems alone. Recent studies have identified two molecular subtypes based on transcriptomic profiling and MYC/TP63 expression (ACC I: MYC-high/TP63-low; ACC II: MYC-low/TP63-high) with potential prognostic significance. However, the magnitude and consistency of their survival impact remain uncertain. A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines. PubMed, Embase, and PubMed Central were searched through January 2026 for studies reporting overall survival in ACC stratified by MYC/TP63 molecular subtype. Hazard ratios (HRs) were pooled using random-effects models. Heterogeneity, subgroup analyses by classification method, sensitivity analyses, cumulative meta-analysis, influence diagnostics, and publication bias assessment were performed. Five independent cohorts from two publications comprising 247 patients (90 ACC I, 157 ACC II) were included. ACC I was associated with significantly worse overall survival compared with ACC II, with a pooled HR of 3.88 (95% CI: 2.55-5.90; < 0.001). No statistical heterogeneity was observed (I = 0%). Prognostic separation was consistent across RNA sequencing and immunohistochemistry-based classification methods. Transcriptomic and MYC/TP63-based molecular subtyping provides strong and reproducible prognostic stratification in ACC. ACC I tumors confer an approximately four-fold higher mortality risk compared with ACC II tumors. Incorporation of molecular subtype into routine diagnostic and clinical decision-making may improve risk stratification, surveillance strategies, and future trial design in ACC. - Source: PubMed
Publication date: 2026/04/29
Rao Karthik NDange PrajwalSreeram M PCoca-Pelaz AndrésStenman GöranFerrarotto RenataShetty TeerthaAgaimy AbbasFerlito Alfio - Split-hand/foot malformation (SHFM) is a serious congenital anomaly. A multitude of pathogenic genes associated with SHFM have been identified; , and are currently recognized. As a transcription factor, TP63 plays an important role in the development of the ectoderm. - Source: PubMed
Publication date: 2026/04/24
Long Jie-YiLiu Qin-ZhiChang Si-HuaWang Run-YanJin Jie-YuanLi NingCheng Zhen-Bo - Natural products and affordable herbal medications have emerged as promising alternatives for cancer therapy, particularly for patients with limited access to standard treatments. Among these, curcumin, the bioactive polyphenol from Curcuma longa (turmeric), has shown broad anti-cancer potential. However, its molecular mechanism remains poorly defined, especially for head and neck squamous cell carcinoma (HNSCC). Here, we identify curcumin as a potent inhibitor of HNSCC tumorigenesis and explored its underlying mechanism. Comparative analyses of three anti-cancer natural products, including curcumin, gingerol, and allicin, revealed that only curcumin robustly inhibited HNSCC cell proliferation, invasion, and cancer stem cell self-renewal, with potency comparable or superior to cisplatin. Transcriptomic and Gene Set Enrichment Analyses demonstrated that curcumin significantly suppressed FOSL1/AP-1 signaling, a well-known key oncogenic signaling that promotes malignant progression of HNSCC. Biophysical and biochemical assays showed that curcumin directly binds to the FOSL1/JUN heterodimer (Kd ≈ 10 μM), disrupting its DNA-binding activity. In agree with this finding, chromatin immunoprecipitation confirmed that curcumin inhibited FOSL1/JUN recruitment to promoter of cancer stem cell marker gene BMI1, as well as super-enhancer-associated oncogenic loci such as MET, EGFR and TP63. At last, curcumin treatment profoundly suppressed HNSCC tumor growth in xenograft model and exhibited superior efficacy compared with the FOSL1/AP-1 inhibitor T-5224, without apparent toxicity. Collectively, our findings identify FOSL1/JUN complex as a direct molecular target of curcumin and uncover a novel mechanism by which this accessible natural product suppresses HNSCC tumorigenesis, supporting its potential as an affordable and safe therapeutic option for cancer treatment. - Source: PubMed
Publication date: 2026/05/07
Li JerryPandit SaritaManupati KanakarajuWang AndrewZaman Shadid UCen Yana - Super-enhancer-associated long non-coding RNAs (lncRNAs) have been shown to play key roles in the occurrence and development of malignant tumors, including esophageal squamous cell carcinoma (ESCC), yet their precise molecular mechanisms remain elusive. - Source: PubMed
Publication date: 2026/05/07
Zheng Ze-JunLiu Yin-QiaoLi Yan-ShangHan Dong-ChenZhu Jun-DeSu Qi-XinWang Zhi-YaLi ChunKang Zhuo-YingGuo Jin-ChengXie Ying-HuaYe Jing-RuMao Lu-ShuangPeng Jiang-YunXiong Xing-DongXie Jian-Jun