ArticleOncology letters2018
Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells.
Article in Oncology letters, 2018. 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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Who cites it
1 citing paper in PubMed.
- Beyond self-reports: serum cotinine reveals sex-and age-related differences of smoking on all-cause and disease-specific mortality.Frontiers in public health · 2025Article
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4 authors.
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Abstract
To determine whether estrogen receptor-α36 (ER-α36) -mediated rapid estrogen signaling is associated with 78 kDa glucose-regulated protein (GRP78) expression in gastric cancer, 86 samples of gastric tumor tissue with corresponding normal and tumor-adjacent tissues were used to examine expression patterns of GRP78 and ER-α36. Immunohistochemistry demonstrated that 55/86 (63.95%) patients with gastric carcinoma, and western blot analysis revealed that GRP78 was upregulated in 15/20 (75%) of tumor specimens. GRP78 expression was positively associated with ER-α36 expression, the male sex and lymph node metastasis (P<0.05). Estrogen treatment increased GRP78 and ER-α36 expression, as well as GSK-3β phosphorylation in established gastric cancer SGC-7901 cells. The steady-state level of GRP78 protein expression and the level of phosphorylated GSK-3β at Ser9 were decreased in SGC-7901 cells with ER-α36 knockdown. Forced expression of ER-α36 in SGC-7901 cells, however, led to an increase in GRP78 expression and GSK-3β phosphorylation. It may therefore be concluded that ER-α36-mediated rapid estrogen signaling positively regulates GRP78 expression, presumably via the GSK-3β pathway, which may be associated with gastric carcinogenesis.
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