ArticleCancer biology & medicine2019
STIM1 overexpression in hypoxia microenvironment contributes to pancreatic carcinoma progression.
Article in Cancer biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Integrin α5β1 in pancreatic ductal adenocarcinoma: Tumour‒stroma crosstalk, hypoxia and therapeutic targeting.Clinical and translational medicine · 2026Review
- Red Blood Cell Aggregation, Angiogenesis and Hypoxia Biomarkers in Pancreatic Cancer.Journal of clinical medicine · 2026Article
- The phenotypic heterogeneity of tumor-derived cells in the bloodstream of pancreatic cancer patients.Frontiers in cell and developmental biology · 2026Article
- STIM1/SOX2 proteins are co-expressed in the tumor and microenvironmental stromal cells of pancreatic ductal adenocarcinoma and ampullary carcinoma.World journal of surgical oncology · 2024Article
- Hyperthermia Influences the Secretion Signature of Tumor Cells and Affects Endothelial Cell Sprouting.Biomedicines · 2023Article
- Implications of Possible HBV-Driven Regulation of Gene Expression in Stem Cell-like Subpopulation of Huh-7 Hepatocellular Carcinoma Cell Line.Journal of personalized medicine · 2022Article
- High expression of hypoxia-inducible factor 1-alpha predicts poor prognosis in pancreatic ductal adenocarcinoma: a meta-analysis and database validation protocol.Translational cancer research · 2022Article
- Article
- Development of a novel multi-functional integrated bioconjugate effectively targeting K-Ras mutant pancreatic cancer.Journal of pharmaceutical analysis · 2022Article
- The relevance between hypoxia-dependent spatial transcriptomics and the prognosis and efficacy of immunotherapy in claudin-low breast cancer.Frontiers in immunology · 2022Article
- Hypoxia-Related Signature Is a Prognostic Biomarker of Pancreatic Cancer.Disease markers · 2022Article
- Effects of Ion-Transporting Proteins on the Digestive System Under Hypoxia.Frontiers in physiology · 2022Review
- CaCancers · 2021Review
- Store-Operated Calcium Entry: Shaping the Transcriptional and Epigenetic Landscape in Pancreatic Cancer.Cells · 2021Review
- Pancreatic Cancer and Its Microenvironment-Recent Advances and Current Controversies.International journal of molecular sciences · 2020Review
- Implications of HIF-1α in the tumorigenesis and progression of pancreatic cancer.Cancer cell international · 2020Review
- Ion Channel Signature in Healthy Pancreas and Pancreatic Ductal Adenocarcinoma.Frontiers in pharmacology · 2020Review
- Mitochondrial Deoxyguanosine Kinase Regulates NADFrontiers in oncology · 2020Article
- Functional consequences of enhanced expression of STIM1 and Orai1 in Huh-7 hepatocellular carcinoma tumor-initiating cells.BMC cancer · 2019Article
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
objectiveStromal interaction molecule 1 (STIM1) overexpression has been reported to play an important role in progression of several cancers. However, the mechanism of STIM1 overexpression and its relationship with hypoxia in pancreatic ductal adenocarcinoma (PDAC) remains unclear.
methodsSTIM1 and HIF-1α expression was tested using immunohistochemistry in tissue microarray (TMA) including pancreatic cancer and matched normal pancreatic tissues, and their relationships with clinicopathological parameters were statistically analyzed. q-PCR, Western blot, ChIP, and luciferase assay were employed to 030 analyze transcriptional regulation between HIF-1α and STIM1 in pancreatic cancer PANC-1 cells.
resultsBoth STIM1 and HIF-1α showed higher positive rates and up-regulated expression in cancer tissues compared to that of normal tissues (
conclusionsIn hypoxia microenvironment, up-regulated expression of STIM1 mediated by HIF-1α promotes PDAC progression. HIF-1α and STIM1 are potential prognostic markers and/or therapeutic targets for PDAC treatment.
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