ArticleDigestive diseases and sciences2015
Heat shock protein A4 controls cell migration and gastric ulcer healing.
Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting the NCAPD3 gene activates EGFR and ASNS as two pivotal contributors to gastric cancer progression.Gastroenterology and hepatology from bed to bench · 2024Article
- A pseudo-value regression approach for differential network analysis of co-expression data.BMC bioinformatics · 2023Article
- Inhibition of DNAJC12 Inhibited Tumorigenesis of Rectal Cancer via Downregulating HSPA4 Expression.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Prenatal Environment That Affects Neuronal Migration.Frontiers in cell and developmental biology · 2019Review
- Bioinformatics analysis of fibroblasts exposed to TGF‑β at the early proliferation phase of wound repair.Molecular medicine reports · 2017Article
- Gankyrin induces STAT3 activation in tumor microenvironment and sorafenib resistance in hepatocellular carcinoma.Cancer science · 2017Article
- Unfolding the Role of Large Heat Shock Proteins: New Insights and Therapeutic Implications.Frontiers in immunology · 2016Review
- A Non-enveloped Virus Hijacks Host Disaggregation Machinery to Translocate across the Endoplasmic Reticulum Membrane.PLoS pathogens · 2015Article
- Combined comparative genomic hybridization and transcriptomic analyses of ovarian granulosa cell tumors point to novel candidate driver genes.BMC cancer · 2015Article
- HSPA4, the "Evil Chaperone" of the HSP Family, Delays Gastric Ulcer Healing.Digestive diseases and sciences · 2015Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AIMS AND
methodsHeat shock protein A4 (HSPA4, also called Apg-2), a member of the HSP110 family, regulates the immune response in the gut. Here, we assessed the involvement of HSPA4 in gastric ulcer healing by using fibroblasts from wild-type and HSPA4-deficient mice, a murine gastric ulcer model, and samples from 65 patients with gastric cancer.
resultsHSPA4 expression was inversely correlated with gastric ulcer healing following endoscopic resection of gastric cancer. In the human gastric mucosa, the expression of HSPA4 was inversely correlated with the expression of stromal cell-derived factor 1 (SDF-1), its cognate receptor CXC chemokine receptor 4 (CXCR4), the stromal cell marker vimentin, and the epithelial-mesenchymal transition regulator Twist. HSPA4 was overexpressed in stromal cells as well as in human gastric cancer cells. HSPA4 deficiency increased the expression of SDF-1 and CXCR4, as well as the number of fibroblast-specific protein 1-positive cells, leading to accelerated ulcer healing in the murine gastric ulcer model. Deletion of HSPA4 promoted cell migration in mouse fibroblasts through increased expression of SDF-1 and Twist.
conclusionHSPA4 regulates the expression of SDF-1 and Twist in fibroblasts, thereby controlling gastric ulcer healing.
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