Ask about this productRelated genes to: MAPK7 antibody
- Gene:
- MAPK7 NIH gene
- Name:
- mitogen-activated protein kinase 7
- Previous symbol:
- PRKM7
- Synonyms:
- BMK1, ERK5
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2014-11-19
Related products to: MAPK7 antibody
Related articles to: MAPK7 antibody
- Medullary thyroid carcinoma (MTC) is a neuroendocrine tumor originating from calcitonin producing C-cells and accounts for 1-5% of thyroid cancers. Total thyroidectomy is curative in localized disease (N0), whereas lymph node metastases (N1) are associated with poorer prognosis. However, the molecular mechanisms driving the metastatic shift remain poorly understood. This study aimed to identify miRNA features linked to metastatic spread in MTC, focusing on the transition from N0 to N1. Co-expression networks were constructed for N0 and N1 tumors, and differential connectivity analysis was used to identify key miRNAs acting as regulatory hubs. Functional annotation of their target genes was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), and Reactome pathway analyses. Validation experiments were carried out in MTC cells to evaluate the effects of selected miRNAs on cell proliferation, survival, and MAPK pathway activation. Network analysis revealed distinct miRNA co-expression patterns between N0 and N1 tumors. Differential network analysis highlighted miR-145-3p as a central regulatory hub, exhibiting 29 altered co-expression changes and a marked loss of connectivity in N1. Target enrichment identified 59 validated genes, including key oncogenic drivers such as MYC, PTEN, BCL2, PIK3CA, AKT1, and MAPK7. In MTC cells, simultaneous inhibition of miR-145-3p together with its top co-expressed miRNAs increased proliferation and survival, and enhanced ERK phosphorylation, indicating MAPK pathway activation and a shift toward a more aggressive phenotype. In conclusion, this study identifies a miRNA regulatory hub centered on miR-145-3p that is associated with metastatic progression and highlights the value of network-based approaches in uncovering mechanisms of cancer dissemination. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/09/09
Citarella AnnaPetti ManuelaBesharat Zein MersiniAlfano CaterinaSplendiani ElenaTrocchianesi SofiaCassandro SaraChiacchiarini MartinaSabato ClaudiaGianno FrancescaAutilio Tanja MilenaBrunetti MartinaCatanzaro GiuseppinaVerrienti AntonellaElisei RossellaCiampi RaffaeleRomei CristinaCastagna Maria GraziaCantara SilviaMarotta VincenzoPezzullo LucianoFarina LorenzoDurante CosimoPo AgneseFerretti Elisabetta - Peritoneal metastases (PMs) represent the most frequent, clinically challenging dissemination pattern in advanced gastric cancer, especially poorly cohesive (PCGC) subtype, and are associated with poor prognosis. We aimed to characterize the transcriptomic landscape of primary gastric tumors (PGTs) and matched PMs to identify differential molecular programs, tumor-microenvironment (TME) features, and potential biomarkers. - Source: PubMed
Publication date: 2026/09/02
Bencivenga MariaSimbolo MicheleGobbo StefanoFranceschi AlessandraSandri AngelaVerlato AlbertoFilippini FedericaSecchettin EricaTedone FabrizioMigliore CristinaLuchini ClaudioEwald JanLawlor Rita TeresaNottegar Alessiade Manzoni Giovanni - Glioma remains a challenging malignancy with limited therapeutic options, and the underlying molecular mechanisms driving its progression are not fully understood. Although has been implicated in various tumors, its role in glioma progression and the associated mechanisms warrant further investigation. This study aims to explore whether suppresses glioma growth and invasion by targeting , thereby regulating matrix metalloproteinases (MMPs) and epithelial-mesenchymal transition (EMT). - Source: PubMed
Publication date: 2026/06/24
Sun TingtingWang GuojinChen YeGeng XinZhu XiaofengZhou Houjun - Breast cancer is the second most common cancer worldwide and remains the leading cause of cancer-related deaths among women. Triple-negative breast cancer (TNBC) represents approximately 15-20% of all breast cancer cases and is characterized by an aggressive clinical course and a high risk of metastasis. Extracellular signal-regulated kinase 5 (ERK5) is a critical biomarker that promotes tumor progression through mechanisms involving cell proliferation, invasion, and metastasis; however, its precise role in epithelial-mesenchymal transition (EMT) in TNBC remains unclear. In this study, we analyzed data from 117 patients with TNBC and found that high ERK5 expression was significantly associated with tumor progression, shorter progression-free survival, and shorter overall survival. RNA sequencing of a highly metastatic TNBC cell line revealed that ERK5 knockdown modulated the expression of various gene clusters, particularly those associated with DNA repair, G2/M checkpoint regulation, and angiogenesis. In addition, ERK5 knockdown in a mouse xenograft model significantly suppressed tumor proliferation and lung metastasis, inhibited tumor cell migration, and reduced the expression of EMT-related proteins. Mechanistically, our data further demonstrated that ERK5 regulates the interaction between cellular JUN (c-JUN) and the vimentin promoter, thereby modulating vimentin expression and downstream signaling pathways. A significant positive correlation between ERK5 and vimentin expression in human TNBC tissue specimens further supported this regulatory association. These findings suggest that ERK5 mediates the recruitment of c-JUN to regulate vimentin expression, thereby promoting EMT and metastasis. Thus, the ERK5/c-JUN/vimentin axis may be a potential therapeutic target to improve clinical outcomes in patients with TNBC. - Source: PubMed
Publication date: 2026/06/17
Chen Chia-ChiChang Shu-JyuanLiang Cheng-LoongNguyen Hieu D HLuo Chi-WenChen Yi-ZiYang Yu-TzuHsu Mei-ChiangMoi Sin-HuaHung Chao-MingPan Mei-Ren - Regulated cell death programs influence melanoma progression and antitumor immunity, yet a robust prognostic model integrating multiple cell-death modalities remains limited. - Source: PubMed
Publication date: 2026/07/03
Wu DanZhou YuzeFang JiahongXie JiahengRen Jie