Ask about this productRelated genes to: COX15 Blocking Peptide
- Gene:
- COX15 NIH gene
- Name:
- cytochrome c oxidase assembly homolog COX15
- Previous symbol:
- -
- Synonyms:
- CEMCOX2
- Chromosome:
- 10q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-03
- Date modifiied:
- 2019-04-23
Related products to: COX15 Blocking Peptide
Related articles to: COX15 Blocking Peptide
- The metabolic reprogramming of tumor microenvironment is a critical driver of colorectal cancer (CRC) pathogenesis. In this context, dysregulated lactate metabolism plays a pivotal role in immunosuppression and therapeutic resistance. Integrating single-cell transcriptomics, spatial transcriptomics, and bulk sequencing datasets, this research delineated the lactate metabolic landscape across colorectal cancer (CRC) tumor ecosystems. Single-cell profiling revealed significant metabolic activity in both the epithelial and myeloid compartments. Consequently, a lactate metabolism score (LMscore) was developed, which is based on four core genes (COX15, SLC25A13, COX10, MPC1). An elevated LMscore has been demonstrated to reprogram epithelial developmental trajectories and reconfigure intercellular communication networks, notably through EFNA1-EPHA3-mediated crosstalk with fibroblasts and endothelial cells. Spatial transcriptomics corroborated intimate spatial colocalization and metabolic pathway co-enrichment between lactate-active epithelia and fibroblasts. Clinically, high LMscore independently predicts a decreased overall survival across multiple cohorts and defines a "cold" tumor immune phenotype. This phenotype is characterized by an accumulation of immunosuppressive cells including M2 macrophages and cancer-associated fibroblasts (CAFs) and a reduction in effector T-cell infiltration. This ultimately results in a refractory response to immune checkpoint blockade. Mechanistically, COX15 emerges as a central regulator of lactate metabolic dysregulation, coinciding with fibroblast-derived TGF-β secretion and immunosuppressive niche formation. Functional validation confirms that COX15 targeting suppresses tumor proliferation. This work establishes LMscore as a clinically robust biomarker for prognostication and immunotherapy response prediction, thereby providing a mechanistic foundation for metabolic reprogramming-targeted combinatorial therapies in CRC. - Source: PubMed
Publication date: 2026/06/19
Lan HaishengLi YangLi HuaGuo JunyuWang CunchuanTang Qianli - Deoxynivalenol (DON) is one of the most prevalent mycotoxins found in livestock feed and is known to impair reproductive physiology and oocyte quality. Melatonin (MEL), a potent antioxidant, has been reported to mitigate DON-induced cytotoxicity during in vitro maturation (IVM) of porcine oocytes and cumulus cells. This study aimed to evaluate the impact of DON and MEL supplementation during IVM on oocyte developmental competence and transcriptomic profiles. Developmental outcomes revealed that exposure to DON (1 μM) significantly reduced oocyte maturation (47.6%), whereas co-treatment with DON (1 μM) plus MEL (1 μM) markedly improved the maturation rate (74.4%). To investigate underlying molecular changes, next-generation sequencing (NGS) was performed, followed by quantitative PCR (qPCR) validation of 14 candidate genes. In cumulus cells, MEL supplementation significantly upregulated ATP5F1E, TCEAL2, and RNase P compared to DON treatment alone. In oocytes, MEL restored the expression of mitochondrial and stress-related genes, including NDUFB6, ATP8, and SEC61A2, while reducing the expression of COX15, ACSL4, CPEB2, and MAP7 genes associated with mitochondrial clearance, ferroptosis, and cytoskeletal stress. These expressions were consistent between NGS and qPCR analyses. Collectively, the results suggest that MEL supplementation during IVM alleviates DON-induced cytotoxicity by enhancing mitochondrial function, reducing oxidative stress, and normalizing gene expression in porcine oocytes and cumulus cells. Moreover, these findings support MEL's potential as a protective agent in mycotoxin-contaminated reproductive systems. - Source: PubMed
Publication date: 2026/05/02
Shen Perng-ChihChen Yan-PingBallantyne RolissaChiang Zhong-FengLee Yen-HuaLee Jai-WeiYu Chi - Mitochondrial disease can result from mutations in the enzymes responsible for biosynthesis of heme a and hemylation of respiratory complex IV of the electron transport chain, also known as cytochrome c oxidase (CcO). One of these enzymes, which is essential for assembly and function of CcO and thus function of the electron transport chain, is heme a synthase, COX15. A previously unknown fatal missense mutation of COX15, c.232G > A (p.Gly78Arg), was recently described in a case report by Galvão de Oliveira et al. Here, we show that the p.Gly78Arg-mimicking substitution in the homologous Cox15 protein in Saccharomyces cerevisiae (Gly95Arg) causes Cox15 protein instability and recapitulates the CcO defect observed in the patient. We demonstrate that the CcO defect observed with this Cox15 variant stems from insufficient heme a synthesis, and consequently, insufficient CcO hemylation and decreased levels of CcO. Our results provide insights into the etiology of the disease caused by this variant, suggesting that Cox15 protein instability and consequent attenuation of heme a synthase function is the main molecular factor behind the resulting multisystemic mitochondrial disorder in humans. - Source: PubMed
Publication date: 2026/04/17
Carroll-Deaton Jayda ABohovych IrynaEmetu Faith TDietz Jonathan VRivett Elise DStanley ElinorHegg Eric LFox Jennifer LKhalimonchuk Oleh - Apigenin, a naturally occurring flavonoid with low toxicity, exhibits anticancer activity, yet its effects on microRNAs (miRNAs) and downstream gene networks in esophageal squamous cell carcinoma (ESCC) remain unclear. Here, we evaluated apigenin's antitumor effects in TE-1 and Eca-109 cells, assessing proliferation, apoptosis, colony formation, and invasion. Differentially expressed miRNAs were identified via small RNA sequencing, and candidate target genes were predicted, annotated using GO and KEGG analyses, and validated by qRT-PCR, revealing miRNA-mediated regulatory mechanisms underlying apigenin's inhibitory effects in ESCC. Apigenin markedly suppressed cell proliferation, clonogenic growth, wound closure, and invasive capacity, while promoting apoptosis in a dose-dependent manner. In TE-1 cells, apigenin upregulated hsa-let-7c-3p, hsa-miR-374c-3p, hsa-miR-3177-3p hsa-miR-4454, and hsa-miR-4728-3p, while downregulating hsa-miR-573, hsa-miR-548az-5p, hsa-miR-33b-5p, hsa-miR-4479, and hsa-miR-3198. Correspondingly, tumor-associated target genes including , , , and were upregulated, whereas , , , and were suppressed. In Eca-109 cells, apigenin altered the expression of distinct miRNAs, including the upregulation of hsa-miR-891-5p, hsa-miR-3170, hsa-miR-4421, and hsa-miR-675-5p and the downregulation of hsa-miR-153, hsa-miR-3188, and hsa-miR-4435, thereby modulating key oncogenic targets such as , , and . Functional enrichment analyses indicated that apigenin-regulated genes are involved in multiple cancer-related pathways across cytoplasmic and nuclear compartments. Overall, these results suggest that apigenin suppresses ESCC progression via coordinated miRNA-mRNA regulation, highlighting its potential as a therapeutic agent. - Source: PubMed
Publication date: 2026/02/28
Amjad NoumanMajid MuhammadSun ZhaojianBasnet RajeshRasool KashafWu LinpingLi Zhiyuan - Chronic tendon injuries, characterized by persistent pain, reduced flexibility, and impaired function, pose a significant clinical challenge. Current therapeutic strategies for these injuries are limited. This study highlighted the crucial role of OXPHOS in maintaining tendon homeostasis and suggested potential therapeutic strategies targeting the OXPHOS pathway. - Source: PubMed
Niu Jie-JieWang LongQi Jia-ChenLu Gui-Jun