Ask about this productRelated genes to: EPSTI1 Blocking Peptide
- Gene:
- EPSTI1 NIH gene
- Name:
- epithelial stromal interaction 1
- Previous symbol:
- -
- Synonyms:
- BRESI1, MGC29634
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-05
- Date modifiied:
- 2016-10-05
Related products to: EPSTI1 Blocking Peptide
Related articles to: EPSTI1 Blocking Peptide
- Although chemotherapy in colorectal cancer (CRC) primarily targets epithelial tumor cells, the epithelial cell-intrinsic mechanisms underlying heterogeneous treatment responses remain poorly understood. We integrated the genomic, transcriptomic, and in vitro drug response profiles of CRC patient-derived tumor organoids (PDTOs) with functional assays to identify epithelial cell-intrinsic determinants of chemotherapy response. An epithelial interferon-stimulated gene (ISG) program, reflecting JAK-STAT pathway activity, was associated with reduced chemosensitivity in PDTOs. Single-cell RNA sequencing data of CRC tumors before and after neoadjuvant chemotherapy showed persistent epithelial ISG expression, with EPSTI1 notably enriched in tumors with incomplete pathological responses. Functional studies demonstrated that EPSTI1 knockdown reduced CRC cell viability and enhanced chemosensitivity. Pharmacologic JAK-STAT inhibition with ruxolitinib suppressed ISG expression and attenuated chemotherapy-induced ISG upregulation. These findings highlight the utility of PDTOs for studying tumor-intrinsic mechanisms of treatment response and identify EPSTI1 as an epithelial modulator of chemosensitivity. - Source: PubMed
Publication date: 2026/08/21
Erkan Erdogan PekcanHämäläinen EmmiKolikova JuliaNikupaavola TiiaSajnani KarishmaKuc KorneliaOjala KalleKukkonen MeijuHermelo IsmaïlKurttila AnttiKoskensalo SeljaTarvainen TimoLeppä AlliKeränen IlonaHaapamäki CarolaKarjalainen EssiCarpelan-Holmström MonikaRenkonen-Sinisalo LauraKoskenvuo LauraPuolakkainen PauliMecklin Jukka-PekkaVäyrynen Juha PVirolainen Elina Nykter MattiAaltonen Lauri AUrbanucci AlfonsoLepistö AnnaRistimäki AriSeppälä Toni T - Nervous necrosis virus (NNV) is a major viral pathogen that causes viral nervous necrosis in a wide range of fish species and poses a serious threat to global aquaculture. However, the antiviral responses of mandarin fish (Siniperca chuatsi) to NNV infection remain poorly understood. In this study, we investigated host antiviral responses using Chinese perch brain (CPB) cell line and in vivo infection models. Transcriptome sequencing of red-spotted grouper nervous necrosis virus (RGNNV)-infected CPB cells revealed extensive transcriptional reprogramming, with numerous interferon-stimulated genes (ISGs) significantly upregulated. Comparative transcriptomic analysis across multiple teleost species identified a conserved set of ISGs induced during RGNNV infection, including CMPK2, RSAD2, DHX58, IRF3, and EPSTI1. Among these genes, CMPK2 showed strong induction in both infected CPB cells and mandarin fish brain tissues. Functional assays further demonstrated that CMPK2 overexpression significantly inhibited RGNNV replication in CPB cells and was accompanied by increased expression of several interferon-related genes. These findings provide the first functional evidence that CMPK2 restricts RGNNV infection in S. chuatsi. Our study highlights a conserved interferon-responsive antiviral module in teleost fish and identifies CMPK2 as a potential antiviral effector involved in host defense against RGNNV infection. - Source: PubMed
Publication date: 2026/07/17
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