EGCG inhibits gastric cancer HGC27 cells invasion and migration by targeting the Hedgehog signaling pathway

Rákkutatás · Nasopharyngeal carcinoma

In HGC27 cells, EGCG treatment inhibited proliferation, colony formation, migration, and invasion in a dose‑ and time‑dependent manner.

Gastric cancer remains a leading cause of cancer‑related mortality worldwide, highlighting the urgent need for effective and low‑toxic therapeutic alternatives. This study investigated the antitumor efficacy of Epigallocatechin gallate (EGCG) in gastric cancer, focusing on the Hedgehog signaling pathway. In HGC27 cells, EGCG treatment inhibited proliferation, colony formation, migration, and invasion in a dose‑ and time‑dependent manner. In a nude mouse xenograft model, oral administration of EGCG (10–50 mg/kg) significantly suppressed tumor growth, achieving an 84.2 % reduction in tumor volume in the high‑dose group, accompanied by favorable histopathological changes. Mechanistically, EGCG down‑regulated core Hedgehog pathway proteins (Shh, Gli1, Ptch1) and downstream effectors, Cyclin D1 and MMP‑9, in both in vitro and in vivo models. In conclusion, EGCG exhibits robust anti‑proliferative and anti‑metastatic activity in gastric cancer HGC27 cells by blocking Hedgehog signaling. These findings provide a compelling preclinical rationale for developing EGCG‑based therapeutic strategies targeting the Hedgehog pathway for gastric cancer treatment.

The study demonstrates that EGCG, a natural polyphenol, can suppress key malignant behaviors of gastric cancer cells by targeting the Hedgehog signaling pathway, suggesting a potential low‑toxic therapeutic strategy for gastric cancer.

Bizonyítékszint: Állatkísérletes. Állatmodellben vizsgálták.

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