Pantoprazole Inhibited Metastasis and Angiogenesis Through Wnt/<em>β</em>-Catenin Signaling Pathway in Gastric Cancer Stem-Like Cells

Adv Biomed Res. 2025 Oct 31;14:124. doi: 10.4103/abr.abr_77_24. eCollection 2025.

ABSTRACT

BACKGROUND: The research on different therapy approaches is critical to find an efficient gastric cancer treatment. The processes of new drug production are very expensive and also take about 15 years. Therefore, the use of existing drugs for treating new diseases may be beneficial in pharmaceutical biotechnology. Thus, we investigated the influence of pantoprazole on Wnt signaling pathway, metastasis, stemness markers, and in vitro tube formation in gastric cancer stem-like cells (GCSCs).

MATERIALS AND METHODS: GCSCs were isolated from MKN-45 cells on a nonadhesive surface. Cell viability, angiogenesis, metastasis, and transcription of CTNNB1, WNT1, SMARCD1, CTNNBIP1, KREMEN1, and SUFU genes and protein levels of CTNNBIP1, SMARCD1, and KREMEN1 were measured by trypan blue, tube formation assays, zymography, the real-time RT-PCR, and Western blotting, respectively.

RESULTS: Our findings represented that pantoprazole decreased the cell viability, angiogenesis, metastasis, and stemness features of GCSCs. Also, pantoprazole had an inhibitory impact on Wnt signaling pathway by modulating the transcription level of CTNNB1, WNT1, SMARCD1, CTNNBIP1, KREMEN1, and SUFU genes and protein level of CTNNBIP1, SMARCD1, and KREMEN1.

CONCLUSIONS: We showed that pantoprazole may reduce the tumorigenicity of GCSCs through the Wnt signaling pathway. Therefore, pantoprazole may be an assistance treatment for gastric cancer therapy.

PMID:41307079 | PMC:PMC12646335 | DOI:10.4103/abr.abr_77_24