Core breast cancer-associated molecules: The Essence

Abstract

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.