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Updated: May 22, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Aloe-emodin suppresses prostate cancer by targeting the mTOR complex 2
Kangdong Liu1, Chanmi Park, Shengqing Li
1The World Class Institute and Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Ochang, Cheongwon 363-883, Republic of Korea.
Abstract:
Phosphatidylinositol 3-kinase (PI3-K) amplification and phosphatase and tensin homolog (PTEN) deletion-caused Akt activation contribute to the development of prostate cancer. Mammalian target of rapamycin complex 2 (mTORC2) is a kinase complex comprised of mTOR, Rictor, mSin1, mLST8/GβL and PRR5 and functions in the phosphorylation of Akt at Ser473. Herein, we report that mTORC2 plays an important role in PC3 androgen refractory prostate cell proliferation and anchorage-independent growth. Aloe-emodin, a natural compound found in aloe, inhibited both proliferation and anchorage-independent growth of PC3 cells. Protein content analysis suggested that activation of the downstream substrates of mTORC2, Akt and PKCα, was inhibited by aloe-emodin treatment. Pull-down assay and in vitro kinase assay results indicated that aloe-emodin could bind with mTORC2 in cells and inhibit its kinase activity. Aloe-emodin also exhibited tumor suppression effects in vivo in an athymic nude mouse model. Collectively, our data suggest that mTORC2 plays an important role in prostate cancer development and aloe-emodin suppresses prostate cancer progression by targeting mTORC2.
Insights
Aloe-emodin, a natural compound, inhibits prostate cancer cell growth by targeting mammalian target of rapamycin complex 2 (mTORC2). This study reveals mTORC2
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Prostate cancer development involves Phosphatidylinositol 3-kinase (PI3-K) pathway dysregulation, including Akt activation.
- Mammalian target of rapamycin complex 2 (mTORC2) is crucial for Akt phosphorylation at Ser473 and prostate cancer cell proliferation.
Purpose of the Study:
- To investigate the role of mTORC2 in prostate cancer progression.
- To evaluate the anti-cancer effects of aloe-emodin on prostate cancer cells by targeting mTORC2.
Main Methods:
- Cell proliferation and anchorage-independent growth assays were performed on PC3 prostate cancer cells.
- Protein analysis, pull-down assays, and in vitro kinase assays were used to assess mTORC2 activity and aloe-emodin's interaction.
- In vivo tumor suppression effects were evaluated in an athymic nude mouse model.
Main Results:
- mTORC2 was found to be important in PC3 androgen-refractory prostate cell proliferation and growth.
- Aloe-emodin inhibited PC3 cell proliferation and anchorage-independent growth.
- Aloe-emodin treatment reduced Akt and PKCα activation and directly inhibited mTORC2 kinase activity, showing in vivo tumor suppression.
Conclusions:
- mTORC2 plays a significant role in prostate cancer development.
- Aloe-emodin demonstrates potential as a therapeutic agent for prostate cancer by inhibiting mTORC2 signaling.
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