OCIAD2 Rabbit Polyclonal Antibody
- Known as:
- OCIAD2 Rabbit Polyclonal Antibody
- Catalog number:
- CAN-5463
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- OCIAD2 Rabbit Polyclonal Antibody
Related genes to: OCIAD2 Rabbit Polyclonal Antibody
- Gene:
- OCIAD2 NIH gene
- Name:
- OCIA domain containing 2
- Previous symbol:
- -
- Synonyms:
- MGC45416
- Chromosome:
- 4p11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-15
- Date modifiied:
- 2018-02-12
Related products to: OCIAD2 Rabbit Polyclonal Antibody
Related articles to: OCIAD2 Rabbit Polyclonal Antibody
- While cisplatin is a widely used and effective chemotherapeutic agent in the treatment of head and neck squamous cell carcinoma (HNSCC), the molecular mechanisms underlying its resistance remain poorly understood. In this study, we identify OCIA domain containing 2 (OCIAD2) as a central mediator of chemoresistance and tumor progression in HNSCC. Through transcriptomic analysis and Co-immunoprecipitation coupled with mass spectrometry, we demonstrate that OCIAD2 modulates integrin signaling by directly interacting with integrin β1. Mechanistic investigations reveal that OCIAD2 does not regulate integrin β1 at the transcriptional level, but instead stabilizes its protein expression by preventing lysosomal degradation and enhancing its recycling. Importantly, OCIAD2 binds to SNX17 and enhances its association with integrin β1, promoting its recycling to lipid raft-enriched regions of the plasma membrane. By maintaining integrin β1 in these lipid raft compartments, OCIAD2 sustains the activation of the FAK-PI3K-AKT-mTOR signaling cascade, thereby fostering cellular resilience and resistance to cisplatin. Moreover, targeting OCIAD2, either through genetic silencing or RNA-based therapies, significantly sensitizes tumors to cisplatin treatment in preclinical models. This study uncovers a previously unrecognized trafficking-dependent mechanism of drug resistance, suggesting that OCIAD2 may serve as a novel therapeutic target to overcome chemoresistance in HNSCC. - Source: PubMed
Publication date: 2026/02/08
Cui LiSi ShanshanYe MinLin PeiZou MeiyanLin YunfanChen XuGuo BingSun WenjuanZhao Xinyuan - The aim of this study was to clarify the significance of DNA methylation alterations in the histological and clinicopathological diversity of pleomorphic carcinoma of the lung. Eleven samples of non-cancerous lung tissue (N), and 10 and 11 samples of non-sarcomatoid and sarcomatoid components of cancerous tissue (T), respectively, were microdissected from formalin-fixed paraffin-embedded specimens of 11 patients with pleomorphic carcinoma of the lung. Genome-wide DNA methylation analysis was performed on all 32 microdissected tissue samples using the Infinium MethylationEPIC BeadChip. Principal component analysis revealed that DNA methylation alterations are associated with lung carcinogenesis and that the diversity of DNA methylation profiles may increase during transition of the non-sarcomatoid component to the sarcomatoid component. Genes showing differences in DNA methylation level between 11 N samples and all 21 T samples regardless of whether they were non-sarcomatoid or sarcomatoid, and whose transcription levels are potentially regulated by DNA methylation, were accumulated in the cadherin, Wnt and angiogenesis pathways. Significant differences in DNA methylation level between non-sarcomatoid and sarcomatoid components potentially resulting in transcription alterations were observed in the OCIAD2, LAMB1 and DKK3 genes. Sarcomatoid component-specific DNA hypomethylation relative to N samples of C2orf27A and COX6C was correlated with clinicopathological parameters such as lymph vessel invasion and higher pathological stage, respectively. Sarcomatoid component-specific DNA hypomethylation of TSKU, PLAU, PLEKHG4, RPSAP52, XBP1 and TRIM2 was correlated with both recurrence-free and overall survival. These data suggest that the DNA methylation alterations associated with sarcomatoid change may participate in malignant progression and determine patient outcome. - Source: PubMed
Publication date: 2025/12/05
Nakagomi TakahiroFujimoto MaoKuriyama ShojiHishida TomoyukiAsamura HisaoAsakura KeisukeKanai YaeArai Eri - Non-small cell lung cancer (NSCLC) is one of the most prevalent malignancies and currently shows a poor clinical prognosis. Type II pneumocyte, as one of the main sources of cancer cells in NSCLC, is important to explore the molecular functions of its related markers for a deeper understanding of NSCLC. - Source: PubMed
Publication date: 2025/11/26
Lin ZhaofanYu HanguangYang KaiXu Huijuan - This study aims to utilize multi-omics high-throughput sequencing data, including ATAC-seq and RNA-seq data from TCGA, GTEx, and GEO databases, to construct predictive and prognostic models for lung adenocarcinoma (LUAD) and identify potential biomarkers. We first obtained LUAD ATAC-seq data from TCGA and identified differential chromatin regions and genes through functional analysis. Differential peaks (DPs) potentially influencing LUAD progression were determined by analyzing patients at different stages, and these DPs were annotated to the genome to obtain differential peak genes (DPGs). We then integrated RNA-seq data from GTEx and TCGA to identify differentially expressed genes (DEGs) at the mRNA level, and by intersecting DEGs with DPGs, we identified 337 consensus genes (CGs). Using random forest and LASSO algorithms, we screened the CGs and constructed a predictive model comprising nine predictive-related genes (Pre-RGs), which was validated with an external dataset (GSE140343). Additionally, through Kaplan-Meier and Cox analyses combined with LASSO, five prognostic-related genes (Pro-RGs) were identified and used to establish a prognostic Cox proportional hazards model, also validated by GSE140343. Single-cell dataset analysis examined the expression of Pre-RGs and Pro-RGs across immune cell types, and further meta-analysis in the LCE database verified their expression differences and prognostic significance. Furthermore, we sequenced cell-free RNAs (cfRNAs) from 50 plasma samples (25 early-stage lung cancer and 25 benign pulmonary disease cases) to validate early cancer detection. Overall, we identified signatures including , , , , , , , , , , , , , and , which show potential as drug targets and biomarkers for predicting LUAD development, prognosis, and early detection. - Source: PubMed
Publication date: 2025/11/10
Lu ZhendongBao PengfeiWang TaiweiHu KairuiZhang LinaYi LingPan YuanmingLi WeiyingLu Zhi JohnWang JinghuiRuan Junzhong - Pancreatic ductal adenocarcinoma (PDAC) ranks among the foremost causes of cancer-associated mortality globally, with a 5-year survival rate of less than 10 %. Ovarian carcinoma immunoreactive antigen domain containing 2 (OCIAD2), which has been previously implicated in ovarian carcinogenesis, has emerged as a potential oncogenic factor. However, its functional role in PDAC remains underexplored. - Source: PubMed
Publication date: 2025/11/04
Pan ZhenyanKong LingmingShi FengyuYing KongjieXie HaonanWu XiulinLin GanglianYao JiangqiaoChen ZiyanWang YiChen GangZhu Qiandong