Ask about this productRelated genes to: ELMO3 Blocking Peptide
- Gene:
- ELMO3 NIH gene
- Name:
- engulfment and cell motility 3
- Previous symbol:
- -
- Synonyms:
- FLJ13824, CED12, ELMO-3, CED-12
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-13
- Date modifiied:
- 2015-09-11
Related products to: ELMO3 Blocking Peptide
Related articles to: ELMO3 Blocking Peptide
- Non-small cell lung cancer remains one of the leading causes of cancer-related mortality worldwide, and identifying molecular markers associated with tumor progression and metastasis is important for improving patient management. This study investigated serum ELMO-3 levels in patients with NSCLC and evaluated their relationship with clinicopathological characteristics. Serum samples from 50 NSCLC patients and 20 healthy controls were analyzed. ELMO-3 concentrations were measured using an enzyme-linked immunosorbent assay. Statistical analyses included non-parametric group comparisons, receiver operating characteristic curve analysis, Kaplan-Meier survival analysis, and multivariate Cox proportional hazards regression. The mean ELMO-3 level was 0.409 ± 0.543, which was used as the cutoff value to categorize patients into low- and high-ELMO-3 groups; 76% of patients were classified as low-ELMO-3 and 24% as high-ELMO-3. The results showed that serum ELMO-3 levels did not differ significantly between NSCLC patients and healthy controls and were not associated with metastatic status. However, a significant association was observed between ELMO-3 expression status and tumor histopathology. Survival analysis demonstrated that distant metastasis and radiotherapy were significantly associated with overall survival. In multivariate analysis, age, operability, distant metastasis, and serum ELMO-3 levels were identified as independent factors associated with survival. These findings suggest that circulating ELMO-3 may have potential prognostic relevance; however, the results should be interpreted with caution and require validation in larger, independent cohorts. - Source: PubMed
Publication date: 2026/04/21
Oğuz Soydinç HilalSerilmez MuratTilgen Yasasever CerenBilgin Doğru ElifGezer UğurKaraman ŞuleSakin Nergiz DağoğluDuranyıldız Derya - Epithelial-mesenchymal transition drives tumor metastasis and therapeutic resistance, yet few treatments have been developed that target this process. Here, we show that ELMO2 represents a specific vulnerability in mesenchymal-like cells. ELMO2 suppression induces excessive autophagy and cell death via FAK activity inhibition. We identify ELMO3 as a functional paralog that compensates for ELMO2 loss, establishing a synthetic lethal interaction. The epithelial-mesenchymal transition core regulator ZEB1 represses ELMO3 transcription in mesenchymal-like cells, rendering them sensitive to ELMO2 blockade. ELMO3 is significantly downregulated in epithelial-mesenchymal transition-associated EGFR inhibitor-resistant cells. Furthermore, the survival of these resistant, mesenchymal-like cells depends on ELMO2/FAK signaling. Through structure-based screening, we identify C52, a small-molecule ELMO2 inhibitor that effectively kills ELMO3-low lung cancer cells and EGFR inhibitor-resistant cells. Our study uncovers an ELMO2-ELMO3 synthetic lethal interaction and establishes ELMO2 as a potential therapeutic target for mesenchymal-like cancer and drug-resistant non-small cell lung cancer. - Source: PubMed
Publication date: 2026/04/17
Li MinXue YingChang YuhanXu FanWu FeizhenTian XinjianHu JieSong YijunYu XufenZhou FeiZhou CaicunCao XinWang MeiHuang Qihong - Diabetes-related vascular complications are characterized by impaired ischemia-driven angiogenesis and delayed wound healing. MicroRNAs (miRNAs) are emerging as powerful targets for multifaceted diseases. We previously identified that miRNA-181c-5p has anti-angiogenic properties, but its role in diabetes is unknown. In a hindlimb ischemia model, streptozotocin-rendered diabetic mice treated with an miRNA-181c-5p inhibitor (anti-miR-181c-5p) exhibited improved blood flow reperfusion and increased arteriolar density, compared with diabetic anti-miR-negative (anti-miR-Neg) control mice. Diabetic anti-miR-Neg mice had reduced perfusion relative to nondiabetic control mice. In a murine wound-healing model, inhibition of miRNA-181c-5p rescued diabetes-impaired wound closure rate and increased capillary density, whereas diabetic anti-miR-Neg wounds healed more slowly than nondiabetic anti-miR-Neg wounds. In vitro, inhibition of miRNA-181c-5p increased endothelial tubule formation and cell migration under high-glucose conditions. Mechanistically, anti-miR-181c-5p elevated VEGFA and VEGFR2 protein expression, ERK2 phosphorylation, and Bcl2 mRNA levels. Whole-transcriptome sequencing identified two genes (Elmo3 and Trib1) that were upregulated in anti-miR-181c-5p-treated hindlimbs and wounds. Luciferase assays confirmed VEGFA as a likely direct target of miR-181c-5p, whereas ERK2, ELMO3, and TRIB1 are indirectly regulated. These findings demonstrate that miRNA-181c-5p inhibition promotes angiogenesis and improves vascular repair in diabetes, identifying miRNA-181c-5p as a potential therapeutic target for preventing diabetic vascular complications. - Source: PubMed
Publication date: 2026/03/31
Solly Emma LLuo YingjunPrimer Khalia RMulangala JocelyneDi Bartolo Belinda ANicholls Stephen JPsaltis Peter JBouman Chen ZhenBursill Christina ATan Joanne T M - The impact of efferocytosis-related genes (ERGs) on the diagnosis of colorectal cancer (CRC) remains unclear. In this study, efferocytosis-associated biomarkers for the diagnosis of CRC were identified by integrating data from transcriptome sequencing and public databases. Finally, the expression of biomarkers was validated by real-time quantitative polymerase chain reaction (RT-qPCR). Our study may provide a reference for CRC diagnosis. - Source: PubMed
Publication date: 2024/08/06
Zhang ShengliangJiang YingShi LeiWei TianningLai ZhiwenFeng XuanLi ShiyuanTang Detao - Obstructive sleep apnea (OSA) incurs a huge individual, societal, and economic burden. Specific and selective targeting of hypoglossal motor neurons could be an effective means to treat OSA. Bioluminescent-optogenetics (BL-OG) is a novel genetic regulatory approach in which luminopsins, fusion proteins of light-generating luciferase and light-sensing ion channels, increase neuronal excitability when exposed to a suitable substrate. Here we develop and validate the feasibility of BL-OG for sleep-disordered breathing (SDB). Upon confirming that diet-induced obese mice represent an excellent SDB model, we employed a method of targeting the hypoglossal nucleus (12 N) by peripherally injecting retrogradely transported rAAV2/Retro. With AAV transduction, the eLMO3 protein is expressed in hypoglossal motor neurons (HMN); administration of CTZ results in production of bioluminescence that in turn activates the tethered channelrhodopsin, leading to an increase in the firing of HMN and a 2.7 ± 0.8-fold increase in phasic activity of the genioglossus muscle, a 7.6 ± 1.8-fold increase in tonic activity, and improvements in hypoventilation and apnea index without impacting sleep structure. This is therefore the first study to leverage the rAAV2/Retro vector to execute the BL-OG approach in SDB, which amplified genioglossus muscle discharge activity and increased airflow in mice after activation. This study marks the pioneering utilization of BL-OG in SDB research. - Source: PubMed
Publication date: 2024/07/18
Wang YixuanLiu XuZhang QingfengZhao DongZhou BeiniPan ZhouZha ShiqianHu Ke