SAMM50 Level as a Prognostic and/or Diagnostic Marker for Breast Cancer Development and Progression
Abstract
(1) MCF7 cells are more resistant to SAM50 and TOM40 knockdown. This could be due to their ability to activate the transcription machinery to compensate for the loss due siRNA. (2) All the cell lines try to compensate for the loss of mitochondrial beta barrel proteins by up regulating the respiratory enzyme COXIV. (#) While suppression of SAM50, TOM40, and VDAC1 could result in suppression of epithelial-mesenchymal transition in MCF7, it would prove counter-productive in MDA468, where the expression of Snail was enhanced after knockdown. (4) Since TOM40 is the main channel of entry of nuclear encoded proteins, its knockdown should result in suppresseion of mitochondrial activity. The results of western blot suggest contrary to this in some cases. This could be a result of negative feedback loops originating from mitochondria, but this hypothesis needs to be investigated in detail.(5) The variation in the level of vimentin between different cell lines suggest that while progression of some metastatic adenocacinomas like those similar to MCF7 type may be treated with mitochondrial protein knockdown, this will result in promoting aggressiveness in other categories of breast tumors.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2011
- Accession Number
- ADA581657
Entities
People
- Shvetank Sharma
Organizations
- Emory University