Discussion:
Lipoic Acid In Breast Cancer
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ironjustice
2017-07-07 21:15:09 UTC
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Lipoic Acid Decreases the Viability of Breast Cancer Cells and Activity of PTP1B and SHP2
ALICJA KUBAN-JANKOWSKA, MAGDALENA GORSKA-PONIKOWSKA and MICHAL WOZNIAK
Department of Medical Chemistry, Medical University of Gdansk, Gdansk, Poland
ANTICANCER RESEARCH 37: 2893-2898 (2017)
doi:10.21873/anticanres.11642

https://tinyurl.com/yc3gqf4j

Abstract.
Background: Protein tyrosine phosphatases PTP1B and SHP2 are potential targets for anticancer therapy, because of the essential role they play in the development of tumors. PTP1B and SHP2 are overexpressed in breast cancer
cells, thus inhibition of their activity can be potentially effective in breast cancer therapy.
Lipoic acid has been previously reported to inhibit the proliferation of colon, breast and thyroid cancer cells.
Materials and Methods:
We investigated the effect of alpha-lipoic acid (ALA) and its reduced form of dihydrolipoic acid (DHLA) on the viability of MCF-7 cancer cells and on the enzymatic activity of PTP1B and SHP2 phosphatases.
Results:
ALA and DHLA decrease the activity of PTP1B and SHP2, and have inhibitory effects on the viability and proliferation of breast cancer cells.
Conclusion:
ALA and DHLA can be considered as potential agents for the adjunctive treatment of breast cancer.

Rapidly-dividing cancer cells have a higher iron requirement than properly-dividing cells.
Tumor cells are, thus, sensitive to decrease of iron (17).
This enables the use of iron chelators as a new concept for the design of cancer treatments.
Lipoic acid is known to possess metal-chelating properties, which could be important mechanism of action of LA in anticancer treatment (18).
In this study, we found an inhibitory effect of ALA and DHLA on cancer cell viability using the MCF-7 breast cancer cell line model.
These findings indicate that lipoic acid can be considered a potential agent for breast cancer therapy.

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Iron-binding drugs targeted to lysosomes: a potential strategy to treat inflammatory lung disorders.
Expert Opin Investig Drugs. 2005 Aug;14(8):997-1008.
Persson HL1, Richardson DR.
Author information
Abstract
In many inflammatory lung disorders, an abnormal assimilation of redox-active iron will exacerbate oxidative tissue damage. It may be that the most important cellular pool of redox-active iron exists within lysosomes, making these organelles vulnerable to oxidative stress. In experiments employing respiratory epithelial cells and macrophages, the chelation of intra-lysosomal iron efficiently prevented lysosomal rupture and the ensuing cell death induced by hydrogen peroxide, ionising radiation or silica particles. Furthermore, cell-permeable iron-binding agents (weak bases) that accumulate within lysosomes due to proton trapping were much more efficient for cytoprotection than the chelator, desferrioxamine. On a molar basis, the weak base alpha-lipoic acid plus was 5000 times more effective than desferrioxamine at preventing lysosomal rupture and apoptotic cell death in cell cultures exposed to hydrogen peroxide. Thus, iron-chelating therapy that targets the lysosome might be a future treatment strategy for inflammatory pulmonary diseases.

PMID: 16050792 DOI: 10.1517/13543784.14.8.997

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2017-08-20 09:39:45 UTC
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