ArticleMolecular medicine reports2017
Overexpression of stromal interaction molecule 1 may promote epithelial‑mesenchymal transition and indicate poor prognosis in gastric cancer.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- Knockdown of STIM1 expression inhibits non-small-cell lung cancer cell proliferationBioengineered · 2019Article
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7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the prognostic significance of stromal interaction molecule 1 (STIM1) expression in gastric cancer (GC) and examine the association between STIM1 and epithelial‑mesenchymal transition (EMT). Immunohistochemical staining was performed to detect STIM1, E‑cadherin, β‑catenin and matrix metalloproteinase‑9 (MMP‑9) in 170 GC and 35 adjacent healthy gastric tissue samples. Positive staining of STIM1, E‑cadherin, β‑catenin and MMP‑9 in GC tissues was significantly greater compared with adjacent healthy tissues (P<0.05). Clinicopathological analysis revealed that STIM1 expression was significantly associated with LNM (P<0.001) and tumor‑node‑metastasis stage (P=0.01). The overall survival rate was significantly reduced in STIM1‑positive compared with STIM1‑negative patients (P=0.043). Cox regression analysis indicated that STIM1 expression and LNM were independent prognostic factors for GC. Chi‑square tests suggested that STIM1 expression in GC tissues was significantly associated with E‑cadherin (P<0.001) and β‑catenin (P<0.001), whereas no association was observed between STIM1 and MMP‑9 expression (P>0.05). In conclusion, the results of the present study suggested that STIM1 may be a valuable prognostic marker in GC patients, and that STIM1 may increase GC motility and invasiveness by promoting epithelial‑mesenchymal transition.
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