SR9009, a synthetic agonist of nuclear receptors, targets the lethal prostate cancer subtype PCS1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. This compound inhibits cancer cell proliferation, migration, and invasion while promoting apoptosis. Unlike traditional therapies, SR9009 specifically reduces the expression of FOXM1 and related genes critical for tumor progression, including CENPA, CENPF, CDK1, CCNB1, CCNB2, and BIRC5. These genes, often overexpressed in prostate cancer, are significantly downregulated upon SR9009 treatment. Studies reveal that SR9009 suppresses tumor growth in vivo, providing an effective option for aggressive PCS1 cancers resistant to standard treatments. The compound acts selectively on cancer cells, sparing healthy prostate tissue, and bypassing androgen receptor pathways, which are common targets for current therapies. This mechanism marks a novel approach to combating castration-resistant and highly malignant prostate cancer cases.
Xu, H., Zhang, J., Zheng, X., Tan, P., Xiong, X., Yi, X., Yang, Y., Wang, Y., Liao, D., Li, H., Wei, Q., Ai, J. and Yang, L., 2022. SR9009 inhibits lethal prostate cancer subtype 1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. Cell Death & Disease.
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Xu, H., Zhang, J., Zheng, X., Tan, P., Xiong, X., Yi, X., Yang, Y., Wang, Y., Liao, D., Li, H., Wei, Q., Ai, J. and Yang, L., 2022. SR9009 inhibits lethal prostate cancer subtype 1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. Cell Death & Disease.
Xu, H., Zhang, J., Zheng, X., Tan, P., Xiong, X., Yi, X., Yang, Y., Wang, Y., Liao, D., Li, H., Wei, Q., Ai, J. and Yang, L., 2022. SR9009 inhibits lethal prostate cancer subtype 1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. Cell Death & Disease.
Xu, H., Zhang, J., Zheng, X., Tan, P., Xiong, X., Yi, X., Yang, Y., Wang, Y., Liao, D., Li, H., Wei, Q., Ai, J. and Yang, L., 2022. SR9009 inhibits lethal prostate cancer subtype 1 by regulating the LXRα/FOXM1 pathway independently of REV-ERBs. Cell Death & Disease.