Ask about this productRelated genes to: SNAI2 antibody
- Gene:
- SNAI2 NIH gene
- Name:
- snail family transcriptional repressor 2
- Previous symbol:
- SLUG
- Synonyms:
- SLUGH1, SNAIL2, SLUGH
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-03
- Date modifiied:
- 2019-04-23
Related products to: SNAI2 antibody
Related articles to: SNAI2 antibody
- Ovarian cancer (OC) remains one of the deadliest gynecological malignancies, largely due to late diagnosis and the emergence of resistance to platinum-based chemotherapy. Long non-coding RNAs (lncRNAs) have recently emerged as key regulators of tumor progression and therapeutic adaptation. In this study, we performed integrative transcriptomic profiling of patient-derived TCGA ovarian tumor samples and carboplatin-resistant A2780 (CBDCA-R-A2780) cells to identify lncRNAs whose dysregulation overlaps between a cell-line resistance model and patient tumors. Our analyses revealed extensive transcriptional remodeling across both datasets, with - consistently emerging as a strongly deregulated transcript. Differential expression analysis showed robust upregulation of - in resistant cells and tumor tissues, accompanied by correlations with epithelial-mesenchymal transition (EMT)-related transcription factors such as and and inverse associations with epithelial markers including . Computational predictions using RIblast identified specific - binding regions with candidate miRNAs and mRNAs, prioritizing EMT-related transcripts (e.g., , , ) with favorable hybridization energies for future validation. Additional prioritized interactors included genes linked to stress response (, ) and invasion (, ). Because A2780 has been discussed as an endometrioid-like/non-serous ovarian cancer model, mechanistic inferences primarily apply to this in vitro context, while TCGA analyses provide associative support rather than mechanistic validation. Collectively, these findings highlight - as a candidate regulator associated with transcriptional reprogramming in OC and a promising prognostic biomarker warranting further functional testing. - Source: PubMed
Publication date: 2026/04/11
Gutierrez AlvaroLarronde CarolinaSilva SaloméCastro ConstanzaMaldonado RodrigoLeón DanielaMachuca JuanIli Carmen GloriaBrebi PriscillaBuchegger KurtViscarra Tamara - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with a five-year survival rate of approximately 13%. Patients with PDAC also have an elevated incidence of venous thromboembolism (VTE), despite prophylactic anticoagulation. Thus, there is an urgent need for therapeutic strategies that target tumor progression and hypercoagulability. Protein S (PS), a physiological anticoagulant encoded by the gene, has recently been shown to inhibit PDAC growth in preclinical models. To further examine the physiological relevance of intratumoral PS in PDAC, we performed a meta-analysis of four independent PDAC patient cohorts obtained from cBioPortal. Patients were stratified based on low versus high intratumoral expression based on below- and above-average mean expression, overall survival, and gene expression of select pro-growth genes, implementing a fixed-effects model. High intratumoral expression was associated with a 41.8% reduction in the risk of death compared with low expression (pooled hazard ratio = 0.581) within 30 months of diagnosis from survival data in three cohorts. Elevated expression correlated with marked downregulation of key genes implicated in PDAC invasion and metastasis, including and in all four cohorts. Collectively, these findings suggest that is a potential prognostic biomarker and molecular regulator in PDAC and thus support further investigation into the dual role of PS in tumor progression. - Source: PubMed
Publication date: 2026/03/25
Prouse TeaganMajumder RinkuMajumder Samarpan - Hepatocellular carcinoma (HCC) stands as one of the most lethal cancers globally, with its treatment constrained by limitations of conventional therapies. In this study, we developed zinc-doped -derived carbon dots (Zn-SaCDs) and encapsulated them within apoptotic bodies (Zn-SaCDs@Ap) to induce targeted, broad-spectrum cell death in hepatocellular carcinoma (HCC). In vitro experiments reveal that Zn-SaCDs@Ap effectively inhibits stemness properties and invasive potential while triggering robust apoptosis in HCC cells. Furthermore, studies on orthotopic liver tumors and subcutaneous tumors in mice showed that Zn-SaCDs@Ap can effectively inhibit tumor growth. It is noteworthy that Zn-SaCDs@Ap can induce various types of cell death, including apoptosis, pyroptosis, and necroptosis. Transcriptome analysis reveals that Zn-SaCDs@Ap treatment markedly activates the expression of the C2H2 zinc finger family transcription factors (KLF7, SALL4, SNAI2, ZNF516), which enhance the expression of key proteins involved in PANoptosis regulation, such as AIM2 and NAIP. In conclusion, Zn-SaCDs@Ap can inhibit the progression of HCC though inducing PANoptosis of tumor cells. Zn-SaCDs@Ap demonstrates potential as a novel therapeutic agent for hepatocellular carcinoma (HCC). - Source: PubMed
Publication date: 2026/03/02
Feng Yi-QianCui Bi-JiaShi BingShi Xin-XiuLi AngZhong Wei-LongLiu Hui-JuanSun TaoZhang Heng - Ferroptosis is an iron-dependent programmed cell death (PCD) implicated in cancer therapy response, yet its transcriptional control remains unevenly characterized and often centered on a limited subset of transcription factors (TFs) rather than systematically addressing TF families. The Activating enhancer-binding Protein-2 (AP-2) family of TFs is a plausible but understudied regulatory node linking oncogenic programs to ferroptosis, with prior research limited to AP-2α and AP-2γ, suggesting anti-ferroptotic and pro-tumorigenic roles. Thus, the present study aimed to provide a family-wide analysis of the relationships between AP-2 and ferroptosis across tumors in which this PCD type is considered biologically and clinically relevant. The research integrates ferroptosis gene modules with AP-2 targetomes, tumor-normal expression comparisons, survival stratification, ferroptosis scoring, cross-cohort functional analyses, and signaling pathway projection extending canonical ferroptosis circuits with AP-2-associated non-canonical elements. Consistent associations between AP-2 expression, prognosis, and ferroptosis score were observed in five tumor cohorts: cervical squamous cell carcinoma, glioblastoma, ovarian serous cystadenocarcinoma, pancreatic adenocarcinoma, and thyroid carcinoma. In addition, cross-cohort clustering highlighted genes enriched in redox- and lipid-metabolism programs linked to apoptosis and autophagy-dependent death. Among the candidates emerging from these analyses, ferroptotic markers (, , and ) and AP-2-linked nodes such as , , , , , , and warrant targeted functional and binding validation to infer whether these associations reflect direct AP-2 regulatory mechanisms. Most importantly, AP-2-centered research appears to be a valuable area for guiding studies of tumor-specific ferroptosis vulnerability or resistance. - Source: PubMed
Publication date: 2026/02/28
Kołat DamianGromek PiotrKciuk MateuszZhao Lin-YongKałuzińska-Kołat ŻanetaKontek RenataPłuciennik Elżbieta - Melanoma is an aggressive and highly metastatic malignancy with significant mortality. Although immune checkpoint inhibitors have improved outcomes in advanced disease, immune resistance remains a critical barrier to durable responses, emphasizing the need to define the molecular mechanisms underlying therapeutic failure. Interleukin (IL)30 has been identified as a cancer progression driver with immunosuppressive function in the tumour-microenvironment. Whether it is involved in melanoma aggressiveness and metastasis is unknown. Immunopathological studies, RNA-Seq and CIBERSORTx analyses of tissue samples from the TCGA-SKCM patient cohort, reveal that IL30 expression is absent in normal skin, while it can be found in melanoma and infiltrating immune cells, mostly macrophages. The putative IL30 receptor complex, IL-6Rα/gp130, is expressed by melanoma cells, which respond to IL30 stimulation with increased proliferation and migration, consistent with IL30-mediated upregulation of metastasis-associated genes, including ANG2, CXCR4, ITGB1, MMP2, NME, SNAI2, VEGFA, VEGFC, and L1CAM. Bioinformatic analysis of IL30 transcript levels in TCGA-SKCM tissue specimens, reveals increased IL30 expression in metastases compared with primary tumors, corroborating the experimental findings at the translational level. IL30 reprograms the melanoma immunophenotype by inducing multiple immune checkpoint molecules, including LSECtin, LGALS3, LGALS9, LAG-3, TIM-3, B7-H4, B7-H3, VISTA, and PD-1. Concurrently, IL30 suppresses T cell function by reducing CD25 and HLA-DR expression on CD4⁺ and CD8⁺ T cells, inhibiting their activation and proliferation, decreasing TNF-α and IFN-γ production, and boosting LAG-3 expression, which strongly correlates with IL30 levels in clinical samples. Collectively, these findings identify IL30 as a critical driver of melanoma dissemination and T cell exhaustion, providing a mechanistic link to immune resistance and failure of combination immunotherapies. - Source: PubMed
Publication date: 2026/03/07
Marchetti SimonaSorrentino CarloFieni CristianoCiummo Stefania LiviaBertuccio EstherCrescenti MariaBonaccorsi IreneFerlazzo GuidoDi Carlo Emma