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Article Addendum
BID-Deficient Breast Cancer MCF-7 Cells as a Model for the Study of Autophagy in Cancer Therapy
Monika Lamparska-Przybysz, Barbara Gajkowska and Tomasz Motyl
volume 2 | issue 1
January/February/March 2006Pages: 47 - 48
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The BH3-only death factors share just the short BH3 domain with the other Bcl-2 family subclasses. With the exception of BID, which might also bind to BAX, they are thought to act by binding to and neutralizing Bcl-2 like survival factors. Camptothecin (CPT)-induced apoptosis in breast cancer MCF-7 cells is associated with activation of cathepsin B and aggregation of BAX and BID on mitochondria. BID knock down protects cancer cells against apoptosis and induces autophagy, manifested with increased expression of Beclin1 and MAP1LC3. The compensatory increase in the concentration of Hrk (another member of the BH3-only protein family) and its co-localization with BCL-2 on organelles in BID(-) breast cancer cells has also been observed. Nonetheless, Hrk is not able to substitute for BID in triggering apoptosis. Its role in autophagy induction is also doubtful, since MAP1LC3 expression was equally high in BID(-)Hrk(-) and BID(-)Hrk(+) breast cancer cells exposed to CPT. We conclude that BID can serve as a molecular switch between apoptosis and autophagy. BID(+) and BID(-) breast cancer MCF-7 cells could be considered to be a useful model for the study of the molecular interdependences between apoptosis and autophagy and the role of both processes in cancer therapy.
Addenda to:
Cathepsins and BID are Involved in the Molecular Switch between Apoptosis and Autophagy in Breast Cancer MCF-7 Cells Exposed to Camptothecin
M. Lamparska-Przybysz, B. Gajkowska and T. Motyl
J Physiol Pharmacol 2005; 56:159-79
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.