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Investigate the impact of ASAP1 on the malignant biological behavior of gastric cancer cells and determine its downstream molecular mechanisms.

June 1, 2024HeliyonOpen Access

Role of ADP ribosylation factor guanylate kinase 1 in the malignant biological behavior of gastric cancer

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Investigate the impact of ASAP1 on the malignant biological behavior of gastric cancer cells and determine its downstream molecular mechanisms.
Evaluated ASAP1 overexpression and knockdown in gastric cancer cells using CCK-8, colony formation, flow cytometry apoptosis assays, and Transwell migration/invasion assays.
Assessed protein markers of apoptosis, epithelial-mesenchymal transition (EMT), matrix metalloproteinases, and AKT/p-AKT signaling by Western blot.
Tested in vivo tumor growth following ASAP1 knockdown in nude mice bearing BGC823 cell-derived xenografts.
ASAP1 was overexpressed in gastric cancer cells, driving proliferation, invasion, and migration while inhibiting apoptosis.
Knockdown of ASAP1 decreased MMP2, MMP9, VEGFA, N-cadherin, vimentin, AKT, and p-AKT levels (P < 0.01) while increasing cleaved caspase-3, cleaved PARP, and E-cadherin.
ASAP1 silencing suppressed gastric tumor xenograft growth in nude mice.

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In vitro and in vivo study demonstrates ASAP1 drives gastric cancer progression and metastasis, suggesting its potential as a therapeutic target.

Luo et al. (2024) studied this question.

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In vitro and in vivo study demonstrates ASAP1 drives gastric cancer progression and metastasis, suggesting its potential as a therapeutic target.