tRF-Pro-CGG Suppresses Cell Proliferation and Promotes Apoptosis in Pancreatic Cancer

Area of Science:

• Molecular Biology
• Oncology
• Biochemistry

Background:

• Pancreatic cancer (PC) remains a significant health challenge with limited effective treatments.
• Aberrant expression of non-coding RNAs, including tRNA-derived fragments (tRFs), is implicated in cancer development.
• The specific role of tRF-Pro-CGG in PC pathogenesis is largely unexplored.

Purpose of the Study:

• To investigate the expression profile of tRF-Pro-CGG in pancreatic cancer.
• To elucidate the functional role of tRF-Pro-CGG in PC cell behavior, including proliferation, migration, invasion, and apoptosis.
• To identify the molecular targets and signaling pathways regulated by tRF-Pro-CGG in PC.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) and next-generation sequencing for expression analysis.
• In vitro functional assays (cell proliferation, colony formation, migration, invasion, apoptosis) in PC cell lines.
• Dual luciferase reporter assays and Western blotting to identify and validate molecular targets and signaling pathways (CSF1, PI3K-AKT).

Main Results:

• tRF-Pro-CGG expression was significantly downregulated in PC tissues and cell lines.
• Overexpression of tRF-Pro-CGG suppressed PC cell proliferation, clonality, migration, and invasion, while inducing apoptosis.
• tRF-Pro-CGG directly targets CSF1 and modulates the PI3K-AKT signaling pathway, impacting key molecules like AKT, P-AKT, and PTEN.

Conclusions:

• tRF-Pro-CGG functions as a tumor suppressor in pancreatic cancer.
• The tumor-suppressive activity is mediated by targeting CSF1 and regulating the PI3K-AKT pathway.
• tRF-Pro-CGG holds promise as a potential diagnostic biomarker and therapeutic target for pancreatic cancer.