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Folate Receptor α Contributes to Radiation Resistance in Neuroendocrine Prostate Cancer by Regulating Redox

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    Folate receptor alpha (FRα) drives resistance to radiation therapy in aggressive prostate cancers like neuroendocrine prostate cancer (NEPC). Targeting the folate-FRα axis may overcome this radiation resistance by maintaining cellular redox balance.

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    Area of Science:

    • Oncology
    • Radiation Oncology
    • Molecular Biology

    Background:

    • Prostate cancer (PC) therapy often involves ionizing radiation.
    • Aggressive neuroendocrine prostate cancer (NEPC) exhibits resistance to radiation, leading to poor outcomes.
    • Mechanisms underlying NEPC radiation resistance are not fully understood.

    Purpose of the Study:

    • To identify novel mechanisms of radiation resistance associated with neuroendocrine differentiation in prostate cancer.
    • To investigate the role of folate receptor alpha (FRα) in radiation resistance and NEPC.
    • To elucidate the signaling pathways regulating FRα expression and its contribution to radioresistance.

    Main Methods:

    • Comparative mass spectrometry of cell surface proteins in radiation-treated vs. untreated prostate cancer cell lines.
    • Functional studies to assess the role of FRα and HIF-1α in radiation resistance.
    • Measurement of intracellular glutathione levels and reactive oxygen species (ROS) buffering capacity.

    Main Results:

    • Folate receptor alpha (FRα) was identified as a key protein involved in radiation resistance.
    • FRα expression is regulated by HIF-1α, which also contributes to NEPC and radiation resistance.
    • The folate-FRα axis sustains intracellular glutathione levels, buffering ROS and promoting cell survival under radiation stress.

    Conclusions:

    • FRα plays a critical, causal role in enabling prostate cancer cells to resist ionizing radiation.
    • The folate-FRα axis is a novel therapeutic target for overcoming radiation resistance in NEPC.
    • Targeting the folate-FRα axis may improve treatment efficacy for patients with aggressive prostate cancers by addressing redox homeostasis in a hypoxic environment.