ReferenceID 382

Rottlerin induces autophagy and apoptosis in prostate cancer stem cells via PI3K/Akt/mTOR signaling pathway

Cancer Lett

Autophagy plays an important role in cellular homeostasis through the disposal and recycling of cellular components. Cancer stem cells (CSCs) play major roles in cancer initiation, progression, and drug resistance. Rottl

Back to Browse

Relationship Network

Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.

Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...

Record Fields

Scalar fields from the final reference record.

Reference Id
382
Evidence Id
16972
Core Evidence Id
16972
Source Reference Id
739
Herb2 Reference Id
HBREF001272
Subject Paper Key
HBIN042467_24125861
Pubmed Id
24125861
Doi
10.1016/j.canlet.2013.10.003
Paper Title
Rottlerin induces autophagy and apoptosis in prostate cancer stem cells via PI3K/Akt/mTOR signaling pathway
Paper Abstract
Autophagy plays an important role in cellular homeostasis through the disposal and recycling of cellular components. Cancer stem cells (CSCs) play major roles in cancer initiation, progression, and drug resistance. Rottlerin (Rott) is an active molecule isolated from Mallotus philippinensis, a medicinal plant used in Ayurvedic Medicine for anti-allergic and anti-helminthic treatments, demonstrates anticancer activities. However, the molecular mechanisms by which it induces autophagy in prostate CSCs have not been examined. The main objective of the paper was to examine the molecular mechanisms by which Rott induces autophagy in prostate CSCs. Autophagy was measured by the lipid modification of light chain-3 (LC3) and the formation of autophagosomes. Apoptosis was measured by flow cytometer analysis. The Western blot analysis was used to examine the effects of Rott on the expression of PI3K, phosphorylation of Akt, phosphorylation of mTOR, and phosphorylation of AMPK in pros CSCs. RNAi technology was used to inhibit the expression of Beclin-1 and ATG-7. Rott induced the lipid modification of light chain-3 (LC3) and the formation of autophagosomes after 24h of Rott treatment in prostate CSCs. Rott-treated prostate CSCs induced transition from LC3-I to LC3-II, a hall mark of autophagy. Rott also induced the expression of Atg5, Atg7, Atg12 and Beclin-1 proteins during autophagy. The knock-down of Atg7 and Beclin-1 blocked Rott-induced autophagy. Furthermore, Rott induced AMPK phosphorylation was blocked by 3-MA, Baf and CHX. In addition, inhibition of AMPK expression by shRNA blocked Rott induced autophagy. In conclusion, a better understanding of the biology of autophagy and the pharmacology of autophagy modulators has the potential for facilitating the development of autophagy-based therapeutic interventions for prostate cancer.
Journal
Cancer Lett
Publish Year
2014
Experiment Subject
prostate cancer stem cells
Experiment Type
Cell Experiment
Phenotype Related
Paper Title Cn
Paper Title En
Rottlerin induces autophagy and apoptosis in prostate cancer stem cells via PI3K/Akt/mTOR signaling pathway
Bilingual Status
semi_complete