ArticleThe Journal of biological chemistry2014
A reciprocal shift in transient receptor potential channel 1 (TRPC1) and stromal interaction molecule 2 (STIM2) contributes to Ca2+ remodeling and cancer hallmarks in colorectal carcinoma cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 109 citations in OpenAlex.
- Potential therapeutic target in oncology: Protein palmitoylation (Review).Oncology reports · 2025Review
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.Frontiers in physiology · 2025Article
- New insights into the stromal interaction molecule 2 function and its impact on the immunomodulation of tumor microenvironment.Cell & bioscience · 2024Review
- Postbiotics of Lacticaseibacillus paracasei CECT 9610 and Lactiplantibacillus plantarum CECT 9608 attenuates store-operated calcium entry and FAK phosphorylation in colorectal cancer cells.Molecular oncology · 2024Article
- Investigation of Trpa1 and Trpc1 Immunreactivities in Colon Adenocarcinomas.Cancer management and research · 2024Article
- Allyl Isothiocianate Induces CaCells · 2023Article
- Too much of a good thing: The case of SOCE in cellular apoptosis.Cell calcium · 2023Review
- Transcriptional Basis of CaCancers · 2023Article
- Function of TRPC1 in modulating hepatocellular carcinoma progression.Medical oncology (Northwood, London, England) · 2023Article
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- GABACells · 2022Article
- The TRPC1 Channel Forms a PI3K/CaM Complex and Regulates Pancreatic Ductal Adenocarcinoma Cell Proliferation in a CaInternational journal of molecular sciences · 2022Article
- Store-Operated CaCancers · 2022Article
- Amyloid Beta Oligomers-Induced CaBiomedicines · 2022Article
- The interplay between physical cues and mechanosensitive ion channels in cancer metastasis.Frontiers in cell and developmental biology · 2022Review
- Comprehensive analysis of transient receptor potential channels-related signature for prognosis, tumor immune microenvironment, and treatment response of colorectal cancer.Frontiers in immunology · 2022Article
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- TRP channel expression correlates with the epithelial-mesenchymal transition and high-risk endometrial carcinoma.Cellular and molecular life sciences : CMLS · 2021Article
- Role of Orai3 in the Pathophysiology of Cancer.International journal of molecular sciences · 2021Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the molecular basis of intracellular Ca(2+) handling in human colon carcinoma cells (HT29) versus normal human mucosa cells (NCM460) and its contribution to cancer features. We found that Ca(2+) stores in colon carcinoma cells are partially depleted relative to normal cells. However, resting Ca(2+) levels, agonist-induced Ca(2+) increases, store-operated Ca(2+) entry (SOCE), and store-operated currents (ISOC) are largely enhanced in tumor cells. Enhanced SOCE and depleted Ca(2+) stores correlate with increased cell proliferation, invasion, and survival characteristic of tumor cells. Normal mucosa cells displayed small, inward Ca(2+) release-activated Ca(2+) currents (ICRAC) mediated by ORAI1. In contrast, colon carcinoma cells showed mixed currents composed of enhanced ICRAC plus a nonselective ISOC mediated by TRPC1. Tumor cells display increased expression of TRPC1, ORAI1, ORAI2, ORAI3, and STIM1. In contrast, STIM2 protein was nearly depleted in tumor cells. Silencing data suggest that enhanced ORAI1 and TRPC1 contribute to enhanced SOCE and differential store-operated currents in tumor cells, whereas ORAI2 and -3 are seemingly less important. In addition, STIM2 knockdown decreases SOCE and Ca(2+) store content in normal cells while promoting apoptosis resistance. These data suggest that loss of STIM2 may underlie Ca(2+) store depletion and apoptosis resistance in tumor cells. We conclude that a reciprocal shift in TRPC1 and STIM2 contributes to Ca(2+) remodeling and tumor features in colon cancer.
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