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Title

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

AuthorsSobradillo, Diego ; Hernández-Morales, Miriam ; Ubierna, Daniel; Moyer, Mary P.; Núñez, Lucía ; Villalobos, Carlos
KeywordsCell proliferation
Calcium imaging
Calcium
Colon cancer
Issue Date2014
PublisherAmerican Society for Biochemistry and Molecular Biology
CitationJournal of Biological Chemistry 289(42): 28765-28782 (2014)
AbstractWe have investigated the molecular basis of intracellular Ca2+ handling in human colon carcinoma cells (HT29) vs. normal human mucosa cells (NCM460) and its contribution to cancer features. We found that Ca2+ stores in colon carcinoma cells are partially depleted relative to normal cells. However, resting Ca2+ levels, agonist-induced Ca2+ rises, store-operated Ca2+ entry (SOCE) and store-operated currents (ISOC) are largely enhanced in tumor cells. Enhanced SOCE and depleted Ca2+ stores correlate with increased cell proliferation, invasion and survival characteristic of tumor cells. Normal mucosa cells displayed small, inward Ca2+-release activated Ca2+ currents (ICRAC) mediated by Orai1. In contrast, colon carcinoma cells showed mixed currents composed of enhanced ICRAC plus a non-selective 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 SOCs in tumor cells whereas Orai2 and 3 are seemingly less important. In addition, Stim2 knockdown decreases SOCE and Ca2+ store content in normal cells while promoting apoptosis resistance. These data suggest that loss of Stim2 may underlie Ca2+ store depletion and apoptosis resistance in tumor cells. We conclude that a reciprocal shift in TRPC1 and Stim2 contributes to Ca2+ remodeling and tumor features in colon cancer.
URIhttp://hdl.handle.net/10261/116907
DOI10.1074/jbc.M114.581678
Identifiersdoi: 10.1074/jbc.M114.581678
issn: 0021-9258
e-issn: 1083-351X
Appears in Collections:(IBGM) Artículos
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