Abstract

Progression of cells through cell cycle consists of a series of events orchestrated in a regulated fashion. Such processes are influenced by cell cycle regulated expression of various proteins where multiple families of transcription factors take integral parts. Among these, the steroid hormone receptors (SHRs) represent a connection between the external hormone milieu and genes that control cellular proliferation. Therefore, understanding the molecular connection between the transcriptional role of steroid hormone receptors and cell cycle deserves importance in dissecting cellular proliferation in normal as well as malignant conditions. Deregulation of cell cycle promotes malignancies of various origins, including breast cancer. Indeed, SHR members play crucial role in breast cancer progression as well as management. This review focuses on SHR-driven cell cycle regulation and moving forward, attempts to discuss the role of SHR-driven crosstalk between cell cycle anomalies and breast cancer.

Highlights

  • Cell cycle progression is a finely regulated process with several checks and balances ensuring that division and proliferation is a favored outcome

  • Two members of this family (Estrogen receptor/ estrogen receptor (ER), and Progesterone receptor/progesterone receptor (PR)) are well documented in breast tumor biology as well as they act as clinically established targets in breast cancer [6]

  • With a brief section covering the structure and general functions of steroid hormone receptors (SHRs), this review focuses on finding the SHR-driven cross-talk between cell cycle and breast cancer

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Summary

INTRODUCTION

Cell cycle progression is a finely regulated process with several checks and balances ensuring that division and proliferation is a favored outcome. “steroid hormone receptors (SHRs)” represent an important group of transcription factors, having roles in cellular growth and proliferation [4] Members of this family act upon binding to a steroid hormone ligand. Two members of this family (Estrogen receptor/ ER, and Progesterone receptor/PR) are well documented in breast tumor biology as well as they act as clinically established targets in breast cancer [6]. A/B: N-terminal domain (NTD): This is a highly variable domain and harbors a little similarity in terms of sequence and size among the SHR members It possesses at least one activator function-1 region (AF-1), that acts in a ligandindependent manner [9, 10]. The motif that has the peptide loop to promote the dimerization of receptors by means of the distal or D box, attaches vaguely with DNA [11, 12]

D: Hinge Region
Findings
DISCUSSION
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