METTL3/YTHDF1-Driven SURF6 Promotes Prostate Cancer Stemness via CDK4

Area of Science:

• Oncology
• Molecular Biology
• Cancer Genetics

Background:

• Prostate cancer (PCa) presents a significant global health burden.
• Novel therapeutic targets are crucial for improving PCa patient outcomes.
• Understanding the molecular drivers of PCa progression is essential.

Purpose of the Study:

• To investigate the role of the SURF6 gene in prostate cancer.
• To elucidate the molecular mechanisms underlying SURF6's function in PCa.
• To evaluate SURF6 as a potential therapeutic target for PCa.

Main Methods:

• Bioinformatics analysis and gene expression profiling.
• Western blotting and functional assays (proliferation, migration, invasion, stemness).
• In vitro and in vivo (xenograft) studies to assess SURF6 modulation effects.

Main Results:

• SURF6 is significantly upregulated in PCa tissues, correlating with poor prognosis.
• SURF6 silencing inhibits PCa cell proliferation, migration, and invasion.
• SURF6 regulates CDK4 expression and cancer stem cell markers (CD44, Nanog).
• METTL3 and YTHDF1 regulate SURF6 via m6A modification.
• SURF6 knockdown inhibits tumor growth and stemness in vivo.

Conclusions:

• SURF6 plays a critical role in promoting prostate cancer progression.
• SURF6 is a potential therapeutic target for improving PCa treatment strategies.
• Targeting SURF6 may offer a novel approach for clinical intervention in PCa.