Related Experiment Video
Updated: Feb 23, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor LATS Biosensor
Published on: September 13, 2018
Carnosol inhibits Hedgehog signaling pathway in both LNCaP and DU145 prostate cancer cell lines
Abstract:
To investigate the effect of carnosol on the Hedgehog (HH) signaling pathway in human hormone-dependent prostate cancer cell line LNCaP and hormone-independent prostate cancer cell line DU145. The expression levels of glioma-associated oncogene homolog 1 (Gli1) and Sonic hedgehog (Shh) in human prostate cancer tissues were detected by immunohistochemistry. After treated with carnosol (0.25-16 μmol/L), the cell survival of LNCaP and DU145 cells were detected by MTT assay. The expression levels of Gli1 and Shh mRNA and protein in the two cells were detected by qRT-PCR and western blot, respectively. The apoptosis was determined by the caspase-3 activity assay. Results showed that Shh and Gli1 were upregulated in cancer tissues. The inhibitory effect of carnosol on cell survival was enhanced with concentration, suggesting both LNCaP and DU145 cells were sensitive to carnosol. The inhibitory effects of carnosol on Gli1 and Shh mRNAs in the hormone-dependent LNCaP prostate cancer cell was stronger than that in the hormone-independent DU145 prostate cancer cells. Carnosol downregulated the expression of Gli1 in nucleus, and Shh in cells. Greater carnosol concentration resulted in lower levels of Gli1 and Shh. Carnosol increased caspase-3 activity in a dose-dependent manner, suggesting that carnosol promotes cell apoptosis. Thus, carnosol can inhibit the proliferation and induce the apoptosis of prostate cancer cells in vitro, and its mechanism might be associated with the inhibiting of HH signaling pathway. Although the inhibitory effect of carnosol on hormone-dependent LNCaP prostate cancer cells is stronger than hormone-independent DU145 prostate cancer cells, carnosol might be a potential drug for hormone-independent prostate cancer.
Insights
Carnosol inhibits prostate cancer cell growth and induces apoptosis by downregulating the Hedgehog (HH) signaling pathway. This compound shows potential as a therapeutic agent, particularly for hormone-independent prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- The Hedgehog (HH) signaling pathway is implicated in prostate cancer development.
- Understanding the molecular mechanisms of prostate cancer is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effect of carnosol on the Hedgehog (HH) signaling pathway in human prostate cancer cells.
- To evaluate carnosol's potential as a therapeutic agent for both hormone-dependent and hormone-independent prostate cancer.
Main Methods:
- Immunohistochemistry was used to detect Gli1 and Shh expression in prostate cancer tissues.
- MTT assay, qRT-PCR, and Western blot were employed to assess cell survival and gene/protein expression.
- Caspase-3 activity assay was performed to determine apoptosis levels.
Main Results:
- Sonic hedgehog (Shh) and glioma-associated oncogene homolog 1 (Gli1) were upregulated in prostate cancer tissues.
- Carnosol inhibited cell survival and proliferation in both LNCaP and DU145 cell lines in a dose-dependent manner.
- Carnosol downregulated Shh and Gli1 expression and increased caspase-3 activity, indicating apoptosis induction.
Conclusions:
- Carnosol inhibits prostate cancer cell proliferation and induces apoptosis, potentially through the inhibition of the HH signaling pathway.
- While carnosol demonstrated stronger effects on hormone-dependent cells, it shows promise as a therapeutic agent for hormone-independent prostate cancer.
Related Concept Videos
Hedgehog Signaling Pathway
lncRNA - Long Non-coding RNAs
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Inhibition of Cdk Activity

