The Critical Interplay of CAF Plasticity and Resistance in Prostate Cancer

Article Oncology

Antiandrogen treatment induces stromal cell reprogramming to promote castration resistance in cancer

Hanling Wang et al.

Summary: Lineage plasticity and phenotype switching of cancer-associated fibroblasts (CAFs) play a role in therapeutic resistance and disease relapse. In this study, it is demonstrated that androgen deprivation therapy (ADT)-induced SPP1+ myofibroblastic CAFs (myCAFs) are key stromal constituents driving the development of castration-resistant prostate cancer (CRPC). The findings highlight the importance of inhibiting the polarization or paracrine mechanisms of these subtypes of CAFs to overcome castration resistance and improve therapeutic outcomes.

CANCER CELL (2023)

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Article Multidisciplinary Sciences

Lineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling

Joseph M. Chan et al.

Summary: Drug resistance in cancer is often associated with tumor cell lineage plasticity. The molecular mechanisms driving this plasticity have not been fully understood. This study shows that prostate cancer plasticity is initiated in a population of cells with mixed luminal-basal phenotype and is dependent on increased JAK and FGFR activity. Single-cell analysis in patients with metastatic disease confirms the presence of mixed-lineage cells with increased JAK/STAT and FGFR signaling.

SCIENCE (2022)

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Article Oncology

Ectopic JAK-STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance

Su Deng et al.

Summary: The JAK-STAT signaling pathway plays a crucial role in promoting lineage plasticity-driven resistance to androgen receptor-targeted therapy in prostate cancer. Targeting JAK-STAT proteins may help overcome this resistance and resensitize tumors to therapy.

NATURE CANCER (2022)

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Article Oncology