ArticleScientific reports2017
Hypoxia-inducible ERO1α promotes cancer progression through modulation of integrin-β1 modification and signalling in HCT116 colorectal cancer cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- ERO1α as a Potential Drug Target for Breast Cancer: A Systematic Review of Current Evidence.International journal of molecular sciences · 2025Pooled it
- Remodelling the tumour microenvironment and beyond: ERO1A as a multifaceted regulator and emerging therapeutic target in cancer.Clinical and translational medicine · 2026Review
- Targeting the Endoplasmic Reticulum Oxidoreductin-1 Alpha-Protein Disulfide Isomerase Redox Interface as a Therapeutic Strategy in Cancer.Biomedicines · 2026Review
- ERO1α regulates colon cancer progression and 5-FU resistance through the miR-451a/ARF1 axis.International journal of colorectal disease · 2025Article
- Endoplasmic reticulum oxidoreductin 1α as a potential therapeutic target in diseases: from oxidative protein folding to pathophysiological mechanisms.Frontiers in pharmacology · 2025Review
- Signaling pathways involved in colorectal cancer: pathogenesis and targeted therapy.Signal transduction and targeted therapy · 2024Review
- Biological mechanisms and clinical significance of endoplasmic reticulum oxidoreductase 1 alpha (ERO1α) in human cancer.Journal of experimental & clinical cancer research : CR · 2024Review
- ERO1α promotes the proliferation and inhibits apoptosis of colorectal cancer cells by regulating the PI3K/AKT pathway.Journal of molecular histology · 2023Article
- Application of CRISPR-Cas9 gene editing technology in basic research, diagnosis and treatment of colon cancer.Frontiers in endocrinology · 2023Review
- Decoding the colorectal cancer ecosystem emphasizes the cooperative role of cancer cells, TAMs and CAFsin tumor progression.Journal of translational medicine · 2022Article
- Article
- Hypoxia and the integrated stress response promote pulmonary hypertension and preeclampsia: Implications in drug development.Drug discovery today · 2021Review
- circ-ACACA promotes proliferation, invasion, migration and glycolysis of cervical cancer cells by targeting the miR-582-5p/ERO1A signaling axis.Oncology letters · 2021Article
- ERO1α mediates endoplasmic reticulum stress-induced apoptosis via microRNA-101/EZH2 axis in colon cancer RKO and HT-29 cells.Human cell · 2021Article
- The NFIB-ERO1A axis promotes breast cancer metastatic colonization of disseminated tumour cells.EMBO molecular medicine · 2021Article
- Endoplasmic reticulum oxidoreductase 1 alpha modulates prostate cancer hallmarks.Translational andrology and urology · 2021Article
- The regulation of Hypoxia-Inducible Factor-1 (HIF-1alpha) expression by Protein Disulfide Isomerase (PDI).PloS one · 2021Article
- Knockdown of PPARδ Induces VEGFA-Mediated AngiogenesisFrontiers in oncology · 2021Article
- Hypoxia-induced epithelial to mesenchymal transition in cancer.Cancer letters · 2020Review
- Proteogenomic Characterization Reveals Therapeutic Vulnerabilities in Lung Adenocarcinoma.Cell · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum disulphide oxidase 1α (ERO1α) is an oxidase localized in the endoplasmic reticulum that plays a role in the formation of disulphide bonds of secreted and cell-surface proteins. We previously showed that ERO1α is overexpressed in various types of cancer and we further identified ERO1α expression as a novel factor related to poor prognosis in cancer. However, the biological functions of ERO1α in cancer remain unclear. Here, we investigated the cell biological roles of ERO1α in the human colon-cancer cell line HCT116. ERO1α knockout (KO) by using CRISPR/Cas9 resulted in decreased tumourigenicity in vivo and reduced cell proliferation only under hypoxia in vitro, which suggested that ERO1α promotes cancer progression specifically in a low-oxygen environment. Thus, we evaluated the function of ERO1α in cell proliferation under hypoxia, and found that under hypoxic conditions, ERO1α KO resulted in a contact-inhibited morphology and diminished motility of cells. We further showed that ERO1α KO induced a change in integrin-β1 glycosylation and thus an attenuation of cell-surface integrin-β1 expression, which resulted in the aforementioned phenotype. Our study has established a previously unrecognized link between ERO1α expression and integrin activation, and thus provides new evidence for the effectiveness of ERO1α-targeted therapy for colorectal carcinoma.
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