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Autophagy in antitumor activity of aloin for breast cancer cells compared with doxorubicin

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Title Autophagy in antitumor activity of aloin for breast cancer cells compared with doxorubicin
 
Creator K. Ahmed, Emad
El-Gendy, Asmaa K.
El-Tantawi, Hala
N. El-Rouby, Mahmoud
M. Said, Mahmoud
M. Ghanem, Hala
Y. Esmat, Amr
 
Subject Aloe vera
Chemosensitivity
Estrogen receptor.
 
Description 252-264
Breast cancer is the most commonly diagnosed cancer and is one of the leading causes of cancer mortality in women
worldwide. Natural product compounds have attracted significant attention for their potent effects against human cancers.
Aloin, a natural phytochemical anthraquinone glycoside extracted from Aloe sp., has been previously reported for its
antitumor activity. Autophagy is a highly conserved process that mediates the degradation of dysfunctional cellular
components, such as senescent proteins and organelles. In the present study, we verified the involvement of autophagy in
tolerance to aloin, especially in breast cancer cells with negative estrogen receptors, and as an alternative pathway to
promote cell death in cells expressing mutant p53 status, which often limits the efficacy and accounts for resistance to
chemotherapy. We studied the effect of aloin on 2 types of breast cancer cell lines, estrogen receptor-positive (T47D) and
triple negative (MDA-MB231), and compared to an anthraquinone analog, doxorubicin (Dox) as a reference compound.
Aloin inhibited the cell growth of both T47D and MDA-MB231 cancer cells, in a time- and dose-dependent manner with a
more pronounced effect in the 72 h exposure regimen, and in the ERĪ±+ breast cell line. The autophagic activity of aloin was
emphasized by the formation of autophagosomes and autolysophagosomes, as early and late autophagic compartments,
respectively, as well as the accumulation of acidic vesicular organelles in the tumor cells. Also, upregulation in the protein
expression of some marker genes of autophagy such as beclin 1 and LC3BII/LC3I, and conversely down-regulation in pmTOR
and p62 was recorded. The results suggest that autophagy can be regarded as one of the mechanistic modes of aloin
cytotoxicity in breast cancer cells that evade apoptosis through genetic mutations in p53.
 
Date 2023-04-03T09:53:38Z
2023-04-03T09:53:38Z
2023-04
 
Type Article
 
Identifier 0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscpr.res.in/handle/123456789/61651
https://doi.org/10.56042/ijeb.v61i04.179
 
Language en
 
Source IJEB Vol.61(04) [Apr 2023]