Cancer is a multifactorial condition with aberrant growth of cells. A substantial number of
cancers, breast in particular, are
hormone sensitive and evolve due to malfunction in the steroidogenic machinery.
Breast cancer, one of the most prevalent form of
cancers in women, is primarily stimulated by
estrogens.
Steroid hormones are made from
cholesterol, and regulation of
steroid/
estrogen biosynthesis is essentially influenced by the steroidogenic acute regulatory (StAR)
protein. Although the impact of StAR in
breast cancer remains a mystery, we recently reported that StAR
protein is abundantly expressed in
hormone sensitive
breast cancer, but not in its non-cancerous counterpart. Herein, we analyzed genomic profiles,
hormone receptor expression, mutation, and survival for StAR and steroidogenic
enzyme genes in a variety of
hormone sensitive
cancers. These profiles were specifically assessed in
breast cancer, exploiting The
Cancer Genome Atlas (TCGA) datasets. Whereas StAR and key steroidogenic
enzyme genes evaluated (
CYP11A1, HSD3B, CYP17A1, CYP19A1, and HSD17B) were altered to varying levels in these
hormone responsive
cancers, amplification of the StAR gene was correlated with poor overall survival of patients afflicted with
breast cancer. Amplification of the StAR gene and its correlation to survival was also verified in a number of
breast cancer studies. Additionally, TCGA
breast cancer tumors associated with aberrant high expression of StAR
mRNA were found to be an unfavorable risk factor for survival of patients with
breast cancer. Further analyses of
tumors, nodal status, and
metastases of
breast cancer tumors expressing StAR
mRNA displayed
cancer deaths in stage specific manners. The majority of these
tumors were found to express
estrogen and
progesterone receptors, signifying a link between StAR and
luminal subtype
breast cancer. Collectively, analyses of genomic and molecular profiles of key steroidogenic factors provide novel insights that StAR plays an important role in the biologic behavior and/or pathogenesis of
hormone sensitive
breast cancer.