SFRP1 induces a stem cell phenotype in prostate cancer cells

Area of Science:

• Oncology
• Molecular Biology
• Cell Biology

Background:

• Prostate cancer (PCa) is a leading cause of cancer death globally.
• Castration-resistant prostate cancer (CRPC) presents significant treatment challenges.
• Stromal paracrine signals are implicated in PCa progression to castration resistance.

Purpose of the Study:

• To investigate the role of exogenous SFRP1 in regulating the stem cell phenotype in prostate cancer.
• To elucidate the molecular mechanisms by which SFRP1 influences prostate cancer progression.

Main Methods:

• Treatment of prostate cancer cells with exogenous SFRP1.
• Analysis of cancer stem cell markers and WNT/β-catenin pathway activity.
• Assessment of pluripotent transcription factors (SOX2, NANOG, OCT4).
• Evaluation of prostate cancer stem cell (PCSC) properties in vitro, including tumorsphere formation, migration, drug resistance, and apoptosis.

Main Results:

• Exogenous SFRP1 significantly increased cancer stem cell markers and WNT/β-catenin pathway target genes.
• SFRP1 upregulated pluripotent transcription factors SOX2, NANOG, and OCT4.
• SFRP1 promoted PCSC properties: enhanced tumorsphere formation, migration, bicalutamide resistance, and reduced apoptosis.

Conclusions:

• SFRP1 acts as a mediator of paracrine signaling, promoting a stem cell phenotype in prostate cancer cells.
• SFRP1 deregulation of the WNT/β-catenin pathway contributes to PCa progression and therapeutic failure.
• Understanding SFRP1's role may lead to novel diagnostic and therapeutic strategies for CRPC.