P4HA3 promotes gastric
cancer cell proliferation and invasion via the PI3K/AKT/mTOR signaling pathway
and regulates glycolytic metabolic reprogramming
Abstract: Background: Dysregulated expression
of prolyl 4-hydroxylase subunit alpha 3 (P4HA3) has been identified in Colon cancer, breast cancer, head and neck cancers,
etc. and is closely associated with tumor progression. However, its specific
roles in gastric cancer (GC), particularly regarding alterations in metabolic
pathways, are remain unknown. Objectives: This study investigated how P4HA3
influences glycolytic metabolic reprogramming and the proliferation and
invasion of gastric cancer cells via the PI3K/AKT/mTOR signaling pathway. Methods: To determine P4HA3 levels in
GC tissues and corresponding cell lines, bioinformatics methods, immunohistochemical
(IHC) staining and Western blotting (WB) were conducted. Furthermore, gain- and
loss-of-function experiments, including cell viability assays (CCK-8),
colony-forming tests, scratch wound assays and Transwell invasion experiments,
were utilized to explore the influence of P4HA3 on GC cell growth,
motility and invasive capacity. Changes in cellular metabolism were assessed
using the Seahorse system (under
normoxic conditions), including measurements of
basal metabolism, glycolytic capacity and mitochondrial respiration (oxidative
phosphorylation), as well as Western blot analysis of key glycolytic proteins. Additionally,
the involvement of the PI3K/AKT/mTOR signaling axis was examined by gene set
enrichment analysis (GSEA), WB analysis and pharmacological inhibition studies.
Results: GC tissues and
cell lines exhibited markedly increased levels of P4HA3, correlating
significantly with decreased overall survival (OS). Experimental data indicated
that P4HA3 facilitated GC cell proliferation, migration and invasion. In
addition, P4HA3 enhanced glycolytic activity and increased the
expression of key glycolysis-related proteins. Unexpectedly, P4HA3 also
increased mitochondrial respiration under the assay conditions, suggesting that
P4HA3 may induce a broader metabolic activation rather than an exclusively
glycolytic shift. Mechanistically, the glycolysis-enhancing effects of P4HA3
were found to require PI3K/AKT/mTOR signaling (as shown by
inhibitor studies). Conclusion: P4HA3 promotes glycolysis via the PI3K/AKT/mTOR
signaling pathway, thereby promoting the progression of gastric cancer.









