Ask about this productRelated genes to: MYBL2 antibody
- Gene:
- MYBL2 NIH gene
- Name:
- MYB proto-oncogene like 2
- Previous symbol:
- -
- Synonyms:
- BMYB, B-MYB
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: MYBL2 antibody
Related articles to: MYBL2 antibody
- Recently, various basic research and clinical studies have revealed the further potential of poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitor Olaparib and histone deacetylase inhibitor Chidamide in lung cancer. However, no research available was found to report whether there is a synergistic effect of Olaparib in combination with Chidamide. This research was conducted to investigate whether there is a synergistic effect between the two drugs and the underlying mechanism in lung cancer cell lines. Here, we treat lung cancer cell lines with Olaparib with or without Chidamide in vivo and in vitro. Based on that, we found that there were synergistic effects between Olaparib and Chidamide. Combined use of them cooperatively downregulated the expression of MYBL2, which was responsible for the downregulation of BRCA1, a main member of DNA damage repair. Simultaneously, Olaparib-induced inhibition of PARP expression leads to the 'synthetic lethality' of cells. On the other hand, MYBL2 may regulate the expression of cycle protein dependent kinase 1, causing G2M cell cycle arrest. Consequently, the combination of Olaparib and Chidamide synergistically induces cell apoptosis through synthetic lethality and cell cycle arrest to exert an antitumor effect. - Source: PubMed
Publication date: 2026/04/13
Zhu LilaJi ZhiWang XiaXin JiaqiMa LijunZhang RunshiDeng TingBa YiLiu Rui - Hepatocellular carcinoma (HCC) presents with poor treatment outcomes, creating an urgent need for novel biomarkers to improve diagnosis, prognosis, and precision medicine. While the MYB family of oncogenes is implicated in cancer, the role and regulatory mechanisms of its member, particularly MYB proto-oncogene like 2 (MYBL2), remain underexplored in HCC. Therefore, this study aimed to systematically validate the clinical significance of MYBL2, elucidate its functional role in tumor progression and drug sensitivity, and identify its upstream regulatory mechanisms using an integrative machine learning and experimental framework. - Source: PubMed
Publication date: 2026/04/22
Yang Ya-LingHuang Ying-HsienLin Hung-Yu - There are currently no clinically validated markers for taxane sensitivity in metastatic castration-resistant prostate cancer (mCRPC), so we aimed to predict docetaxel response from circulating cell-free DNA. We identified 180 patients with pre-treatment plasma specimens collected within 12 months of starting docetaxel for mCRPC at our institution. 138 underwent ultra-low pass whole genome sequencing (ULP-WGS), and tumor fractions (TFx) and copy number alterations (CNAs) were derived using ichorCNA. 79 samples with TFx > 0.04 underwent targeted panel sequencing (TPS). TP53 mutation was significantly associated with docetaxel non-response (p = 0.018); deletions involving bands located in arms 11p, 11q, 10q and 3p were enriched in responders, and amplifications in regions of 1p and 6q were enriched in non-responders. Transcription factor (TF) binding activity was inferred using Griffin, which identified TFs (ZSCAN4, CTCF, PHOX2B) with trends towards increased activity in non-responders (n = 22) and others (including PBX1, MYBL2, OSR2, PDX1 and ZIC2) in responders (n = 24). A combined ensemble binary classifier generated through XGBoost integrating these feature sets to predict docetaxel response outperformed models derived from any single feature set, achieving a training area-under-the-ROC curve of 0.87. Pre-cabazitaxel specimens, representing a docetaxel-resistant population, were used for external validation, with a concordance of 79.6% for predicting non-response. - Source: PubMed
Publication date: 2026/04/28
Chen David DZimmer AnatYang David DFrancini EdoardoPatton RobertCrowdis JettChandra PoojaBin Riaz IrbazHanratty BrianRickles-Young MicahTsuji JunkoCibulskis CarrieFleharty MarkWhelpley BridgetReardon BrendanPark JihyeNelson Peter SHuang Franklin WVan Allen Eliezer MHa GavinChoudhury Atish D - Oral squamous cell carcinoma (OSCC) commonly arises from oral potentially malignant disorders (OPMDs), yet reliable molecular biomarkers that predict malignant transformation remain scarce. Because epithelial carcinogenesis follows similar multistep trajectories across multiple organs, pan-cancer transcriptional analyses may reveal conserved pathways relevant to early oral tumorigenesis. This study aimed to identify shared transcriptional signatures across carcinomas and evaluate their applicability to precancerous-to-carcinoma progression. Bulk RNA-seq data from five carcinomas (lung, colon, breast, prostate, and head and neck squamous cell carcinoma, HNSCC) were obtained from TCGA to identify shared differentially expressed genes (DEGs) (|logFC| ≥ 2; FDR < 0.05). Functional enrichment, clustering, and gene-pathway network analyses characterized conserved biological processes. Independent GEO datasets containing premalignant and malignant samples, including OPMD and OSCC cohorts, were examined to assess early-stage relevance. A conserved 45-gene signature was identified, enriched for transcriptional regulation, chromatin organization, and RNA polymerase II-mediated processes. Regulatory hubs, including ZIC5, MYBL2, ONECUT2, POU4F1, and PDX1, and strong upregulation of cancer-testis antigens (MAGEA3, MAGEA6, MAGEC2) were notable. Integration with premalignant datasets revealed 13 genes consistently dysregulated across early lesions, involving pathways such as cell differentiation, apoptosis, and lipid transport. Several genes remained altered from normal tissue through OPMD to OSCC, supporting their potential as stable biomarkers. This study identifies conserved transcriptional programs shared across epithelial cancers and detectable in OPMDs. These findings highlight promising biomarker and regulatory candidates for improving early detection and risk stratification of oral precancer, addressing a critical unmet need in OSCC prevention and clinical management. - Source: PubMed
Publication date: 2026/04/13
Kazemi Kimia SadatMiyazawa MartaHanemann João Adolfo CostaIonta MarisaOliveira Pollyanna Francielli deLeask AndrewFranca Cristiane MirandaSperandio Felipe Fornias - Zinc, an essential trace element for healthy prostate, which dramatically decreases during prostate tumorigenesis. Targeting the key zinc signaling will be a valuable strategy for PCa therapy. However, the underlying mechanisms are poorly understood. Here, we show that zinc is significantly decreased in prostate cancer (PCa), especially in metastatic PCa. Screening reveals that a zinc transporter Zip7 was upregulated in metastatic PCa and related to poor progression. Zip7 silencing inhibits PCa cell migration and invasion in vitro and bone-metastasis in vivo. Mechanistically, we identify that Zip7 mainly interacts with MAZ in cytoplasm to facilitate MAZ nuclear import and nuclear MAZ was up-regulated in metastatic prostate cancer tissues and positively associated with Zip7 expression, which promotes PCa bone metastasis. Furthermore, our RNA-seq studies reveal that Zip7 facilitates MAZ nuclear import to promote MYBL2 transcription. Strikingly, we show in intraarterial injected-bone metastasis xenograft model that targeting Zip7 by its inhibitor markedly suppressed PCa bone metastasis. Collectively, our findings identify Zip7 is an important regulator of PCa metastasis and targeting Zinc-dependent Zip7-MAZ-MYBL2 could be a valuable strategy to ameliorate advanced PCa metastasis. - Source: PubMed
Publication date: 2026/04/20
Dong QianxiXiong YunqiangXiong SituYuan RuizeLi ShengZhan XiangpengHu HongjiZheng FuchunPang WanFu BinXu SonghuiGuo Ju