Decreased long non-coding RNA MTM contributes to gastric cancer cell migration and invasion via modulating MT1F

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
• The specific functions of lncRNAs in gastric cancer (GC) are an active area of research.
• MTM is a cancer-related lncRNA whose involvement in GC progression requires further investigation.

Purpose of the Study:

• To investigate the expression profile of the lncRNA MTM in gastric cancer.
• To explore the correlation between MTM levels and clinicopathological features of GC.
• To elucidate the functional role of MTM in GC cell behavior and identify its potential molecular targets.

Main Methods:

• Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess MTM expression in GC cell lines and tissues.
• Analysis of MTM expression in relation to clinicopathological factors.
• In vitro cell biological assays, including overexpression and co-transfection, to study MTM function.
• Correlation analysis between MTM and MT1F expression levels.

Main Results:

• MTM expression was significantly decreased in GC cell lines and tissues compared to normal controls.
• Lower MTM levels were strongly associated with lymphatic metastasis, invasive depth, tumor stage, and poorer overall survival.
• Overexpression of MTM suppressed GC cell proliferation, migration, invasion, and induced apoptosis.
• A positive correlation was observed between MTM and MT1F expression in GC samples.
• MT1F overexpression inhibited GC cell migration and invasion; MT1F knockdown reversed MTM-induced inhibition, identifying MT1F as a key target of MTM.

Conclusions:

• Downregulation of MTM is a common event in human gastric cancer.
• MTM functions as a tumor suppressor in GC by inhibiting cell migration, invasion, and proliferation.
• MTM may exert its tumor-suppressive effects, at least partly, through the modulation of MT1F expression, suggesting a novel therapeutic target for GC.