MiR-646 inhibited cell proliferation and EMT-induced metastasis by targeting FOXK1 in gastric cancer

Area of Science:

• Molecular Biology
• Oncology
• Gene Regulation

Background:

• Aberrant microRNA-646 (miR-646) expression is noted in various human cancers.
• The specific role and molecular mechanisms of miR-646 in gastric cancer (GC) remain largely uninvestigated.

Purpose of the Study:

• To elucidate the function and molecular mechanisms of miR-646 in gastric cancer.
• To determine if miR-646 acts as a tumor suppressor in GC.

Main Methods:

• In vitro assays (EdU, colony formation, matrigel invasion) were used to assess miR-646's function in GC cells.
• Real-time PCR and Western blotting analyzed miR-646 and FOXK1 expression.
• In vivo studies in nude mice evaluated tumor growth and metastasis.
• Correlation analysis between miR-646 and FOXK1 expression in human GC tissues.

Main Results:

• miR-646 expression was significantly downregulated in GC tissues compared to normal adjacent tissues.
• Overexpression of miR-646 inhibited GC cell proliferation, migration, and epithelial-mesenchymal transition (EMT).
• miR-646 directly targets FOXK1, inhibiting its pro-proliferative and EMT-inducing effects; inverse correlation observed in human GC tissues.
• miR-646 regulates the Akt/mTOR signaling pathway downstream of FOXK1.

Conclusions:

• miR-646 functions as a tumor suppressor in gastric cancer.
• miR-646 inhibits GC cell proliferation and EMT progression by directly targeting FOXK1.
• These findings highlight miR-646 as a potential therapeutic target for gastric cancer.