ArticleScientific reports2021
SHH-N non-canonically sustains androgen receptor activity in androgen-independent prostate cancer cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Transcriptomic analysis to uncover the mechanism of radiosensitization of AR-positive triple-negative breast cancers with AR inhibition.NPJ breast cancer · 2026Article
- Mortalin promotes the evolution of androgen-independent prostate cancer through Wnt/β-catenin signaling pathway.Cancer cell international · 2024Article
- GLI Transcriptional Targets S100A7 and KRT16 Show Upregulated Expression Patterns in Epidermis Overlying the Tumor Mass in Melanoma Samples.International journal of molecular sciences · 2024Article
- 'Toxic Masculinity': What Is Known about the Role of Androgen Receptors in Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2023Review
- Higher Expressions of SHH and AR Are Associated with a Positive Receptor Status and Have Impact on Survival in a Cohort of Croatian Breast Cancer Patients.Life (Basel, Switzerland) · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
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Abstract
Prostate cancer is the second most frequent cancer diagnosed in men worldwide. Localized disease can be successfully treated, but advanced cases are more problematic. After initial effectiveness of androgen deprivation therapy, resistance quickly occurs. Therefore, we aimed to investigate the role of Hedgehog-GLI (HH-GLI) signaling in sustaining androgen-independent growth of prostate cancer cells. We found various modes of HH-GLI signaling activation in prostate cancer cells depending on androgen availability. When androgen was not deprived, we found evidence of non-canonical SMO signaling through the SRC kinase. After short-term androgen deprivation canonical HH-GLI signaling was activated, but we found little evidence of canonical HH-GLI signaling activity in androgen-independent prostate cancer cells. We show that in androgen-independent cells the pathway ligand, SHH-N, non-canonically binds to the androgen receptor through its cholesterol modification. Inhibition of this interaction leads to androgen receptor signaling downregulation. This implies that SHH-N activates the androgen receptor and sustains androgen-independence. Targeting this interaction might prove to be a valuable strategy for advanced prostate cancer treatment. Also, other non-canonical aspects of this signaling pathway should be investigated in more detail and considered when developing potential therapies.
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