Icariin plus curcumol enhances autophagy through the mTOR pathway and promotes cathepsin B-mediated pyroptosis of prostate cancer cells
10.4103/apjtb.apjtb_649_23
- Author:
Xu-Yun Wang
1
;
Wen-Jing Xu
2
;
Bo-Nan Li
3
;
Tian-Song Sun
3
;
Wen Sheng
4
Author Information
1. Department of Andrology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, 100010, China
2. Department of Dermatology, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, 410021, China
3. School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China; Andrology Laboratory, Hunan University of Chinese Medicine, Changsha, 410208, China
4. School of Rehabilitation Medicine and Health Care, Hunan University of Medicine, Huaihua, 418000, China; School of Traditional Chinese Medicine, Hunan University of Medicine, Huaihua, 418000, China
- Publication Type:Journal Article
- Keywords:
Icariin;
Curcumol;
Autophagy;
mTOR;
Cathepsin B;
Pyroptosis;
Prostate cancer
- From:Asian Pacific Journal of Tropical Biomedicine
2024;14(2):55-64
- CountryChina
- Language:English
-
Abstract:
Objective: To examine the effect of icariin plus curcumol on prostate cancer cells PC3 and elucidate the underlying mechanisms. Methods: We employed the Cell Counting Kit 8 assay and colony formation assay to assess cell viability and proliferation. Autophagy expression was analyzed using monodansylcadaverine staining. Immunofluorescence and Western blot analyses were used to evaluate protein expressions related to autophagy, pyroptosis, and the mTOR pathway. Cellular damage was examined using the lactate dehydrogenase assay. Moreover, cathepsin B and NLRP3 were detected by co-immunoprecipitation. Results: Icariin plus curcumol led to a decrease in PC3 cell proliferation and an enhancement of autophagy. The levels of LC3- Ⅱ/LC3-Ⅰ and beclin-1 were increased, while the levels of p62 and mTOR were decreased after treatment with icariin plus curcumol. These changes were reversed upon overexpression of mTOR. Furthermore, 3-methyladenine resulted in a decrease in inflammatory cytokines, pyroptosis-related protein levels, and lactate dehydrogenase concentration, compared to the icariin plus curcumol group. Inhibiting cathepsin B reversed the regulatory effects of icariin plus curcumol. Conclusions: Icariin plus curcumol demonstrates great potential as a therapeutic agent for castration-resistant prostate cancer by enhancing autophagy via the mTOR pathway and promoting pyroptosis mediated by cathepsin B. These findings provide valuable insights into the molecular mechanisms underlying the therapeutic potential of icariin and curcumol for prostate cancer treatment.
- Full text:20240202.pdf
