Researchers investigated the role of Hedgehog-GLI signaling in sustaining androgen-independent growth of prostate cancer cells.
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Colorectal cancer cells hijacked prostaglandin E2 (PGE2) to non-canonically promote Hedgehog transcriptional factor Gli activity and Gli-dependent proliferation of colorectal cancer cells in a Smo-independent manner.
[Cell Death & Disease]
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Scientists revealed that the smoothened cascade was upregulated in benign prostatic hyperplasia tissues and was localized in both the stromal and the epithelium compartments of human prostate tissues.
[Cell Death Discovery]
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Researchers identified a novel SOX2-BRD4 transcriptional complex driving the expression of GLI1, the final effector of the Hedgehog/GLI (HH/GLI) pathway, providing a novel mechanism of non-canonical Smoothened-independent activation of HH/GLI signaling in melanoma.
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Pietrobono, S., Gaudio, E., Gagliardi, S., Zitani, M., Carrassa, L., Migliorini, F., Petricci, E., Manetti, F., Makukhin, N., Bond, A. G., Paradise, B. D., Ciulli, A., Fernandez-Zapico, M. E., Bertoni, F., & Stecca, B. (2021). Targeting non-canonical activation of GLI1 by the SOX2-BRD4 transcriptional complex improves the efficacy of HEDGEHOG pathway inhibition in melanoma. Oncogene, 1–16. https://doi.org/10.1038/s41388-021-01783-9 Cite
Scientists assessed the expression of key genes involved in hedgehog signaling in prostate cancer and investigated the potential role of smoothened in the pathogenesis of neuroendocrine prostate cancer.
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Investigators found that mesenchymal stem cell CD47 and macrophage signal regulatory protein alpha expression were increased after LPS stimulation.
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Researchers demonstrated that malignant melanoma cell motility was impaired by targeting carbonic anhydrase IX via either carbonic anhydrase inhibitors or through the inhibition of the Hedgehog pathway.
The authors used single cell RNA-sequencing of patient tumors to identify three prognostic surface markers (LYPD3, TACSTD2, and LY6D) which correlated with myocardin-related transcription factor (nMRTF) and resistance to Smoothened inhibitors. The nMRTF cell state resembled transit-amplifying cells of the hair follicle matrix, with AP-1 and TGFß cooperativity driving nMRTF activation.
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Yao, C. D., Haensel, D., Gaddam, S., Patel, T., Atwood, S. X., Sarin, K. Y., Whitson, R. J., McKellar, S., Shankar, G., Aasi, S., Rieger, K., & Oro, A. E. (2020). AP-1 and TGFß cooperativity drives non-canonical Hedgehog signaling in resistant basal cell carcinoma. Nature Communications, 11(1), 5079. https://doi.org/10.1038/s41467-020-18762-5 Cite
Smoothened (SMO) expression correlates with tumor size, invasiveness, metastasis and recurrence. In addition, SMO inhibitors can suppress cancer formation, reduce the proliferation of cancer cells, trigger apoptosis and suppress cancer stem cell activity.
[International Journal of Medical Sciences]
Investigators showed that novel combinations of JAK2 inhibitors with SMO inhibitors synergistically inhibited in vitro growth of TNBC and HER2-positive trastuzumab-resistant BT474-TtzmR cells.
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Doheny, D., Sirkisoon, S., Carpenter, R. L., Aguayo, N. R., Regua, A. T., Anguelov, M., Manore, S. G., Arrigo, A., Jalboush, S. A., Wong, G. L., Yu, Y., Wagner, C. J., Chan, M., Ruiz, J., Thomas, A., Strowd, R., Lin, J., & Lo, H.-W. (2020). Combined inhibition of JAK2-STAT3 and SMO-GLI1/tGLI1 pathways suppresses breast cancer stem cells, tumor growth, and metastasis. Oncogene, 1–17. https://doi.org/10.1038/s41388-020-01454-1 Cite
Colony formation assay and flow cytometry were used to evaluate the effect of garcinone C on the proliferation and cell cycle progression of colon cancer cells.
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