EMP_1 (Epithelial Membrane Protein) Formula C94H133N25O26S2 Sequence Gly_Gly_Thr_Tyr_Ser_Cys_His_Phe_Gly_Pro_Leu_Thr_Trp_Val_Cys_Lys_Pro_Gln_Gly_Gly
- Known as:
- EMP_1 (Epithelial Membrane Protein) Formula C94H133N25O26S2 Sequence Gly_Gly_Thr_Tyr_Ser_Cys_His_Phe_Gly_Pro_Leu_Thr_Trp_Val_Cys_Lys_Pro_Gln_Gly_Gly
- Catalog number:
- 88512
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- GLSChina
- Gene target:
- EMP_1 (Epithelial Membrane Protein) Formula C94H133N25O26S2 Sequence Gly_Gly_Thr_Tyr_Ser_Cys_His_Phe_Gly_Pro_Leu_Thr_Trp_Val_Cys_Lys_Pro_Gln_Gly_Gly
Related genes to: EMP_1 (Epithelial Membrane Protein) Formula C94H133N25O26S2 Sequence Gly_Gly_Thr_Tyr_Ser_Cys_His_Phe_Gly_Pro_Leu_Thr_Trp_Val_Cys_Lys_Pro_Gln_Gly_Gly
- Gene:
- CLDN1 NIH gene
- Name:
- claudin 1
- Previous symbol:
- -
- Synonyms:
- SEMP1, ILVASC
- Chromosome:
- 3q28
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-19
- Date modifiied:
- 2016-10-05
- Gene:
- EMP1 NIH gene
- Name:
- epithelial membrane protein 1
- Previous symbol:
- -
- Synonyms:
- TMP, CL-20
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-05
- Date modifiied:
- 2015-03-31
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EtBr)/protein (ex. SYPRO Ruby) gel imaging""Recombinant Human Limbic system-associated membrane protein_LSAMP""Recombinant Human Limbic system-associated membrane protein_LSAMP""Recombinant Human Limbic system-associated membrane protein_LSAMP" Related articles to: EMP_1 (Epithelial Membrane Protein) Formula C94H133N25O26S2 Sequence Gly_Gly_Thr_Tyr_Ser_Cys_His_Phe_Gly_Pro_Leu_Thr_Trp_Val_Cys_Lys_Pro_Gln_Gly_Gly
- Chemoresistance remains a major obstacle to improving outcomes in colorectal cancer (CRC), particularly among patients receiving 5-fluorouracil (5-FU)-based therapy. Here, we developed a READ-derived response-associated gene signature for recurrence stratification and performed exploratory cross-cohort evaluation in additional colorectal cancer cohorts, while further exploring its association with treatment-response phenotypes. In the GSE190826 cohort, pathological complete response (pCR) versus non-pCR status was used as a clinically annotated treatment-response phenotype for downstream screening. Using differential expression analysis in TCGA-READ, we identified 4277 differentially expressed genes and constructed a weighted gene co-expression network analysis (WGCNA) to define clinically relevant modules. Genes from READ-related modules were further screened by logistic regression in GSE190826 and univariate Cox regression in TCGA-READ, yielding six prognostic genes associated with pathological non-response. Least absolute shrinkage and selection operator (LASSO)-Cox regression subsequently refined these candidates to a four-gene signature, including ENHO, BLACAT1, LEMD1, and ASNS, which was used to establish a READ-derived response-associated gene (RDRG) risk score. High-risk patients showed poorer recurrence-free survival in the TCGA-READ training set and an exploratory TCGA-READ testing subset, and exploratory evaluations in additional colorectal cancer cohorts (TCGA-COAD and GSE17536) showed similar recurrence-stratification trends, with moderate time-dependent AUC values in TCGA-READ (3-year AUC = 0.766; 5-year AUC = 0.714). Multivariate Cox analyses showed that the risk score remained associated with RFS after adjustment for clinical covariates, and a nomogram incorporating disease stage provided additional exploratory prognostic stratification. The RDRG score also showed only modest and exploratory associations with treatment-response phenotypes across multiple datasets. Single-cell RNA-seq analysis revealed that malignant cells contributed the highest risk scores, with enrichment of epithelial-mesenchymal transition (EMT), KRAS signaling, coagulation, and hypoxia-related programs in high-risk tumor cells. Among the four genes, LEMD1 showed the strongest malignant-cell enrichment and was further examined in functional assays, where LEMD1 knockdown reduced CRC cell migration and increased 5-FU sensitivity, supporting its role as a candidate functional contributor rather than a validated mechanistic driver. Collectively, the RDRG risk score may serve as a READ-derived model for recurrence stratification, with exploratory cross-cohort applicability in broader colorectal cancer cohorts and exploratory associations with treatment-response phenotypes. The same risk-score formula was applied across cohorts, whereas high- and low-risk thresholds were cohort-specific rather than fixed from the training cohort. - Source: PubMed
Publication date: 2026/08/17
Li ShuaiLi JingxianBu XianyueHan MeiShi Ganggang - Oxidized low density lipoprotein receptor 1 (OLR1) regulates glycolytic metabolism, lactate production and carcinogenesis, but its role in papillary thyroid cancer (PTC) is still unclear. The present study aimed to investigate the effect of OLR1 modification on PTC cellular functions and its interaction with histone H3 lysine 18 lactylation (H3K18la) and downstream molecular mechanisms. Lectin‑like oxidized low‑density lipoprotein receptor‑1 (LOX‑1; OLR1 coding protein) and H3K18la expression was detected in twenty pairs of PTC and non‑tumor tissues by immunohistochemistry. Overexpressed OLR1 and small interfering (si)RNA were transfected into two PTC cell lines (TPC‑1 and IHH‑4 cells). After which, oxamate (to reduce lactate production) or LEM domain containing 1 (LEMD1) siRNA combined with OLR1 overexpression plasmid was used to treat PTC cell lines. Furthermore, PTC xenograft mice were constructed for verification. LOX‑1 and H3K18la expression was upregulated in PTC tissues versus non‑tumor tissues and LOX‑1 expression positively associated with H3K18la expression in PTC tissues. OLR1 overexpression facilitated cell proliferation and invasion but repressed cell apoptosis in PTC cell lines, while OLR1 siRNA revealed an opposite effect. OLR1 positively regulated lactate production, H3K18la expression and LEMD1 expression. Furthermore, a chromatin immunoprecipitation assay confirmed a direct binding between H3K18la and the LEMD1 promoter. H3K18la expression was lowered by oxamate‑induced lactate reduction, which also attenuated the effect of OLR1 overexpression on PTC cell proliferation, apoptosis and invasion and downregulated LEMD1 expression. Moreover, LEMD1 siRNA weakened the effect of OLR1 overexpression on PTC cell proliferation, apoptosis and invasion. experiments revealed that OLR1 overexpression elevated tumor volume and weight and upregulated the expressions of LEMD1 and H3K18la; while LEMD1 knockdown reduced tumor volume and weight. In conclusion, OLR1 promotes PTC proliferation and invasion, while represses apoptosis through regulating H3K18la‑mediated LEMD1. - Source: PubMed
Publication date: 2026/08/14
Yu JiaweiPang RuiLiu BoChen LiliZhang Jiewu - Andrographis has anti-cancer activity in various human cancers, including colorectal cancer. Our aim was to explore the detailed mechanisms underlying Andrographis in colorectal cancer progression. Andrographis inhibited the proliferation, reduced the invasive ability, and induced apoptosis in LoVo and HCT-116 cells. LEM domain containing 1 (LEMD1) expression was upregulated in colorectal cancer cells and tissue samples, and Andrographis significantly decreased LEMD1 expression in LoVo and HCT-116 cells. LEMD1 knockdown restrained colorectal cancer development by inhibiting proliferation and invasion and triggering apoptosis. Krüppel-like factor 3 (KLF3) targeted LEMD1 and positively regulated its expression in colorectal cancer cells. KLF3 overexpression reversed the anti-tumor effects of Andrographis on LoVo and HCT-116 cells, and this reversal was attenuated by LEMD1 silencing. Additionally, Andrographis hampered tumor growth and downregulated KLF3 and LEMD1 expression in colorectal cancer mice. In conclusion, Andrographis exerts anti-tumor activity in colorectal cancer through decreasing KLF3 and LEMD1 expression. - Source: PubMed
Publication date: 2026/05/09
Zhang LeyiLi DongyangTang YanXie Yicheng - Nuclear envelope dysfunction is increasingly recognized as a driver of cancer-associated alterations in chromatin organization, genome stability, and mechanotransduction. Among inner nuclear membrane components are the LEM-domain (LEM-D) proteins LAP2/TMPO, emerin (EMD), LEMD1, LEMD2, MAN1/LEMD3, ANKLE1, and ANKLE2. Accumulating evidence links dysregulation of these proteins to hallmark cancer processes, including cell-cycle control, epithelial-mesenchymal transition, genome instability, and therapeutic resistance. This review synthesizes recent mechanistic and translational findings on LEM-D proteins in cancer, highlighting isoform-specific functions, context-dependent oncogenic versus tumor-suppressive roles, and convergence on key pathways such as Wnt/β-catenin, PI3K/AKT, MAPK, and TGF-β signaling. Concrete evidence for prognostic value varies across the LEM-D proteins. While much of the current evidence derives from transcript-level and preclinical studies, emerging data suggest that LEM-D proteins contribute to nuclear stress adaptation and may represent context-dependent therapeutic vulnerabilities. We discuss their prognostic and predictive potential, critically evaluate limitations in current datasets, and present a unifying framework linking LEM-D dysfunction to genome instability, altered signalling, and therapy resistance. Thus, despite growing evidence of therapeutic potential, these proteins are better positioned as biomarkers to guide current therapies. - Source: PubMed
Publication date: 2026/04/22
Jobe AmieMirza SameerVijayan Ranjit - LAP2-emerin-MAN1 (LEM) domain-containing protein 1 (LEMD1), first identified in colorectal cancer in 2004, is a gene that is specifically expressed in the testis. The expression of LEMD1 is minimal in normal somatic cells but high in various types of malignant tumor (such as gastric, prostate, pancreatic and colorectal cancer as well as oral squamous cell carcinoma) due to abnormal promoter demethylation. LEMD1 promotes cell proliferation, invasion and metastasis during tumor progression, making it a potential diagnostic marker and therapeutic target. The present review summarized the research progress of LEMD1 as a cancer-testis antigen in tumor biology. Furthermore, the present review investigated the molecular structure and biological functions of LEMD1, its expression patterns, clinical relevance in various types of tumor, and highlighted current research challenges and future directions. - Source: PubMed
Publication date: 2026/04/01
Wang Xiao-BoWang Xian-FeiAbdul Karim Sairah Binti