ArticleAnimal cells and systems2020
Upregulating miR-637 aggravates endoplasmic reticulum stress-induced apoptosis in gastric cancer cells by suppressing Calreticulin.
Article in Animal cells and systems, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Identification of immunogenic cell death-related prognostic genes in gastric cancer.Journal of gastrointestinal oncology · 2026Article
- Predictive value of miR-637 for the occurrence of myocardial hypertrophy in patients with hypertension.Journal of cardiothoracic surgery · 2025Article
- The dual effect of endoplasmic reticulum stress in digestive system tumors and intervention of Chinese botanical drug extracts: a review.Frontiers in pharmacology · 2024Review
- Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023Review
- Galectin‑1 binds GRP78 to promote the proliferation and metastasis of gastric cancer.International journal of oncology · 2022Article
- Dysfunction and ceRNA network of the tumor suppressor miR-637 in cancer development and prognosis.Biomarker research · 2022Review
- Calreticulin enhances gastric cancer metastasis by dimethylating H3K9 in the E-cadherin promoter region mediating by G9a.Oncogenesis · 2022Article
- Comprehensive Analysis of Endoplasmic Reticulum Stress in Intracranial Aneurysm.Frontiers in cellular neuroscience · 2022Article
- Kazinol C fromAnimal cells and systems · 2022Article
- Dysregulation of miR-637 serves as a diagnostic biomarker in patients with carotid artery stenosis and predicts the occurrence of the cerebral ischemic event.Bioengineered · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer is a leading cause of cancer death worldwide. Endoplasmic reticulum (ER) stress-induced apoptosis has been confirmed to be important in the treatment of gastric cancer. MiR-637 has recently been found to exert inhibitory effects on gastric cancer, and this study aimed to investigate whether miR-637 could regulate apoptosis through ER stress. The results showed that tunicamycin (TM) induced downregulation of miR-637 in gastric cancer cells (AGS) and increase of apoptosis and ER stress. Overexpression of miR-637 promoted TM-induced apoptosis and expression of ER stress associated proteins (GRP78 and CHOP), but inhibited expression of Calreticulin. MiR-637 could bind with the 3'-UTR of
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