ArticleHuman cell2025
HSPA8 promotes the progression of gastric cancer by activating the canonical Wnt pathway and glycolysis.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Article
- Integrated genome-wide high-throughput screening and functional validation identifies Sm proteins as essential splicing regulators for gastric cancer progression.Functional & integrative genomics · 2026Article
- Urinary metabolomics and proteomics for early detection of gastric cancer: insights from a two-center multicenter study.Frontiers in oncology · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HSPA8, a crucial molecular chaperone, has been implicated in the promotion of cancer across various malignancies. The clinical significance of HSPA8 in gastric cancer (GC) and its molecular contribution to tumour progression are unknown. Sequencing data from the GEO and TCGA databases, along with independent immunohistochemical data, revealed that HAPA8 was upregulated in GC tissues and was associated with tumour stage. HSPA8 knockdown decreased GC cell proliferation, migration, and invasion in vitro. According to the results of transcriptome sequencing and western blotting, HSPA8 suppression primarily affects the Wnt/β-catenin signalling and glycolysis pathways. In nude mice, HSPA8 knockdown drastically reduced tumour growth. The results of the current study validated the oncogenic function of HSPA8 in GC. Its overexpression is linked to GC development and poor clinicopathology.
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Registered trials
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