Targeting Key Metabolic Enzymes Involved in Lipid and Protein Biosyntheses for Breast Anticancer Therapies.
The evolution of genomic research enabled the genetic and molecular profiling of breast cancer and revealed the profound complexity and heterogeneity of this disease. Subtypes of breast cancer characterized by mutations and/or amplifications of some proto-oncogenes are associated with an increased rate of recurrence and poor prognosis. They represent a challenge in the clinic with limited arsenal to attack them. Nowadays, metabolic reprogramming is firmly established as a hallmark of cancer. An increased rate of lipid and protein syntheses in cancerous tissues, a direct consequence of alterations in key metabolic enzymes involved in these pathways, is now recognized as an important aspect of the rewired metabolism of neoplastic cells. Over the past several years, accumulating evidence has revealed that mutations or amplifications of some proto-oncogenes are primarily involved in this metabolic dysregulation. It is thus critically important to dissect the molecular mechanisms tumors use to link metabolic reprogramming with upstream altered signaling. In this article, we review the recent findings that support the importance of lipid and protein biosyntheses in breast tumorigenesis, discuss the crosstalk between growth factor signal transduction and key metabolic enzymes involved in these processes, and point out the potentials of developing new strategies and therapeutics to target these key parameters in order to help breast cancer patients by providing new therapeutic opportunities.
Mounia
M
Guerram
Aida Mejda
AM
Hamdi
Lu-Yong
LY
Zhang
Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, No. 24, Tongjiaxiang, Nanjing 210009, Jiangsu Province, PR China. Select country.
Zhenzhou
Z
Jiang
D001943:Breast Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D004798:Enzymes / Q000378:metabolism*; D005260:Female; D006801:Humans; D050356:Lipid Metabolism; D058990:Molecular Targeted Therapy / Q000379:methods; D014176:Protein Biosynthesis; D011506:Proteins / Q000378:metabolism*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism
D004798:Enzymes; D011506:Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases; C508053:ERBB2 protein, human
Breast cancer; lipid; metabolism; protein; proto-oncogenes; targeted therapy