CORE BREAST CANCER ASSOCIATED MOLECULES: The Essence
DOI:
https://doi.org/10.14456/tjg.2013.144Keywords:
BRCA1, c-Myc, CyclinD1, ER-related molecules, survivinAbstract
Various cellular factors in which their proliferative functions are inter-related (i.e., genes, proteins, miRNA) have been increasingly reported, both in normal cell and cancer. Increase in cellular proliferative rate in cancer is attributed to deregulation of mechanisms related to cell cycle, tumor suppressor and apoptotic control pathways. In this regard, there must be some error occurring within the functional molecules in one or more of these pathways. For instances, gene mutation or amplification, chromosome aberration, epigenetic change, abnormal increase or decrease of some miRNA or derangement of interacting proteins. In breast cancer, alike other cancers, cell cycle driving genes usually express at the level higher than normal and sometimes known as “proliferative or cancer signature” genes. Noteworthy, some cancer-associated genes express at a low level in cancer and are not recognized as the proliferative or cancer signature in spite of their obvious roles on tumorigenesis. The genes include those known to express for cell cycle inhibitors, intercellular adhesive molecules, proteins which function for DNA repairing and genome stability and molecules that contribute in apoptosis. This review gathers and concludes the roles of key molecules believed to be breast cancer associated to date. Cumulative knowledge of molecular cross-talking signals in normal mammary epithelium guides us to understand how deviated molecules and distorted regulations occur in breast cancer. In addition, no single molecule can provide full cellular proliferative function and this is also true in cancer. Hence, targeted therapy for cancer with highly specific inhibitor to such a single molecule expected to be the leading cancer actor is generally not guarantee of the therapeutic successful, and should be performed with careful consideration.
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