Elk1 (Ab_417) Antibody
- Known as:
- Elk1 (Ab_417) Antibody
- Catalog number:
- E021038-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Elk1 (Ab_417) Antibody
Related genes to: Elk1 (Ab_417) Antibody
- Gene:
- ELK1 NIH gene
- Name:
- ETS transcription factor ELK1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-01-21
Related products to: Elk1 (Ab_417) Antibody
Related articles to: Elk1 (Ab_417) Antibody
- Bladder cancer (BC) is one of the most common malignancies of the urinary system, and chemoresistance remains a major obstacle limiting the clinical efficacy of cisplatin-based chemotherapy. Elucidating the mechanisms underlying cisplatin resistance may facilitate the identification of potential therapeutic targets and ultimately improve patient outcomes. In this study, we found that Y-box binding protein 1 (YBX1) was upregulated in bladder cancer tissues with poor chemotherapeutic response as well as in cisplatin-resistant bladder cancer cell lines, where it promoted tumor cell proliferation and invasion. Functional assays demonstrated that depletion of YBX1 significantly enhanced cisplatin sensitivity in both in vitro and in vivo. Mechanistically, elevated YBX1 expression was associated with reduced ferroptosis sensitivity in cisplatin-resistant cells. Although YBX1 induced autophagy and was accompanied by a reduction in glutathione peroxidase 4 (GPX4) protein levels, the overall enhancement of intracellular antioxidant capacity in resistant cells may partially offset the increased susceptibility to ferroptosis caused by GPX4 degradation. Furthermore, we identified the transcription factor ELK1 as an upstream regulator that transcriptionally upregulates YBX1, while YBX1 may contribute to the cisplatin-resistant phenotype through activation of the p62-NRF2-associated antioxidant pathway. Collectively, these findings highlight a critical role of YBX1 in cisplatin resistance and suggest that targeting YBX1 may represent a promising strategy for overcoming cisplatin-based chemoresistance in bladder cancer. - Source: PubMed
Publication date: 2026/06/01
Luo YaoMa JunhaiWang ChengXiong WeiZhang XingxingZhang BiaoFu YuqiangZhang XiaojunWang JienengZhang HelinZheng YanghuangLu JianzhongShang Panfeng - Brain metastasis represents an advanced complication in non-small cell lung cancer (NSCLC), characterized by therapeutic resistance and dismal survival outcomes. Although astrocytes are known to influence tumor progression within the brain microenvironment, their prognostic significance and mechanistic contributions to NSCLC brain metastasis (NSCLC-BM) remain largely unresolved. In this study, we analyze brain metastatic tumors from 66 patients with NSCLC and demonstrate that high infiltration of astrocytes is significantly associated with reduced overall survival. Functional assays reveal that astrocytes enhance the stemness of metastatic tumor cells, a phenotype that is significantly attenuated by silencing astrocytic monocarboxylate transporter 1 (MCT1), thereby blocking lactate uptake. Mechanistically, lactate reprograms astrocytes to release extracellular vesicles enriched in miR-8085, which downregulates the E3 ubiquitin ligase TRIM67 in tumor cells. This suppression stabilizes the transcription factor ELK1 through inhibition of ubiquitin-mediated degradation, promoting stemness maintenance and tumorigenic capacity. Clinically, low TRIM67 and high ELK1 expression correlate with poorer survival in patients with NSCLC-BM. Together, our findings uncover a novel lactate-induced miR-8085/TRIM67/ELK1 signaling cascade that drives brain metastasis progression and highlight potential prognostic biomarkers and therapeutic targets for patients with NSCLC involving the brain. - Source: PubMed
Publication date: 2026/05/31
Peng HaiqinTanzhu GuilongShi WenXiao GangZeng QianChen LiuWan XinJing DiDeng HaibinMarti Thomas MichaelFu JunZhou Rongrong - Premature ovarian insufficiency (POI) not only affects fertility, but also has a profound impact on women's general health, mental health and quality of life. This research was designed to explain the function and mechanism of wild-type and edited miR-483-5p in POI. Western blot analysis and RT-qPCR were utilized to evaluate gene expression. Human granulosa cell activities were assessed via CCK-8, colony formation, EdU and TUNEL assays. FSH, E2, and AMH levels were measured using ELISA. Commercially available kits were obtained to detect glucose uptake and ROS level. The targets of miRNAs were confirmed through dual-luciferase reporter assay. High editing level of miR-483-5p induced by ADAR1 enzyme was related to high FSH level and low E2, AMH levels in POI patients. Functionally, miR-483-5p restrained granulosa cell proliferation and elevated apoptosis. Interestingly, A-to-I RNA editing aggravated miR-483-5p effect on granulosa cell activity. In vivo experiment also demonstrated that edited and wild-type miR-483-5p exacerbated POI by regulating granulosa cell proliferation and apoptosis. Mechanically, A-to-I RNA editing alters the targets of miR-483-5p. And ed-miR-483-5p obtains novel target ESR2 and loses ELK1. Specifically, miR-483-5p promoted POI progression by intensifying ELK1-mediated oxidative stress. Edited miR-483-5p aggravated POI development by downregulating ESR2-mediated hormone synthesis and glycometabolism. A-to-I RNA editing reinforces the pathogenicity of miR-483-5p in POI by regulating hormone synthesis and glucose metabolic mechanism through altering its target ELK1 as ESR2. - Source: PubMed
Publication date: 2026/05/26
Ma NieyingXu KaijieLiu JuanWang Zhize - Gastric cancer (GC)-derived exosomes (Exos) have been identified to facilitate GC progression by inducing M2 macrophage polarization. This study investigated the biological function of exosomal matrilin-3 (MATN3) in M2 macrophage polarisation during GC development and its underlying mechanism. Exos were isolated from GC cells and then co-cultured with THP-1-derived macrophages. Macrophage polarisation was evaluated by measuring the levels of M1/M2 macrophage markers. Target molecule expression was evaluated by RT-qPCR, Western blotting and immunohistochemical staining. LC3II expression and the co-localisation of MATN3 and epidermal growth factor receptor (EGFR) were determined by immunofluorescent staining. In vivo growth of GC cells was assessed in a xenograft mouse model. Molecular mechanisms were analysed by Co-IP, ChIP, dual-luciferase reporter assay and ubiquitination assay. MATN3 was highly expressed in GC and its high expression was negatively associated with the overall survival and M1 macrophage marker expression of GC patients. The in vitro experiments validated that MATN3 was secreted by GC-Exos, which promoted M2 macrophage polarisation via autophagy activation. In addition, exosomal MATN3 contributed to in vivo growth of GC cells via promoting M2 macrophage infiltration. Mechanistically, MATN3 interacted with EGFR to enhance its protein stability, which activated Ets-like protein-1 (ELK1) and consequently promoted ATG12-mediated autophagy. Activation of the EGFR/ELK1 pathway abolished exosomal MATN3 silencing-mediated inhibitory effect on autophagy and M2 macrophage polarisation. GC-derived exosomal MATN3 exerted an oncogenic role by inducing M2 macrophage polarisation via activation of the EGFR/ELK1/ATG12 axis-mediated autophagy, which provides potential therapeutic targets for GC. - Source: PubMed
Publication date: 2026/05/20
Zhao QianwenLiu ShanshanShe XinMa ShiyueTang HuiPeng DanliGuo Haonan - Non-small cell lung cancer (NSCLC) is characterized by high incidence, mortality, and poor patient prognosis, with chemotherapy resistance being a common challenge. This research intends to identify key molecules involved in NSCLC and elucidate the regulatory role of the LINC01605/miR-7111-5p/ELK1 axis in chemotherapy resistance. LINC01605 and its downstream targets were predicted using the lncRNASNP2-human and miRDB databases. RT-qPCR was employed to measure the expression of LINC01605 across different NSCLC patients, and its prognostic value was assessed through ROC curve, Kaplan-Meier curve, and Cox regression. Dual-luciferase reporter assay was conducted to verify interactions between miR-7111-5p and LINC01605 or ELK1. Transwell assay evaluated cell invasion capabilities, while CCK8 assay confirmed changes in chemotherapy drug sensitivity in chemotherapy-resistant cells across different treatment groups. Elevated expression of LINC01605 was observed in NSCLC patients, correlating with reduced survival rates, and its expression was further elevated in patients with chemotherapy resistance. The upregulation of miR-7111-5p inhibited the proliferation and invasion of NSCLC cells induced by LINC01605. Mechanistically, LINC01605 negatively regulated miR-7111-5p expression while positively influencing ELK1 expression. Silencing ELK1 and upregulating miR-7111-5p levels reversed the chemotherapy resistance of A549 cells induced by LINC01605. By targeting the miR-7111-5p/ELK1 regulatory axis, LINC01605 induced chemotherapy resistance in NSCLC, highlighting its potential as a significant biomarker for NSCLC. - Source: PubMed
Publication date: 2026/05/15
Zhang FangYang Zhi-LiangQin Tian-TianZhang Guo-JunLi Xiang