
The Role of STAT1 in T Helper Cell Differentiation during Breast Cancer Progression
Author(s) -
Sayantan Banik,
Sudeshna Rakshit,
Koustav Sarkar
Publication year - 2021
Publication title -
journal of breast cancer/journal of breast cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 36
eISSN - 2092-9900
pISSN - 1738-6756
DOI - 10.4048/jbc.2021.24.e34
Subject(s) - medicine , breast cancer , oncology , cancer research , cancer
Members of the signal transducer and activator of transcription (STAT) protein family are intracellular transcription factors that facilitate several facets of cellular immunity, proliferation, apoptosis, and differentiation. They are principally stimulated by membrane receptor-associated Janus kinases. Dysregulation of this pathway is often detected in primary tumors and hints at augmented angiogenesis, which enriches tumors persistence and immunosuppression. STAT proteins play indispensable roles in cytokine signaling and T helper (Th) cell differentiation. Among STAT proteins, STAT1 plays a vital role in interferon signaling, which initiates the expression of genes encoding proteins with antitumor and apoptotic roles. STAT1 signaling is essential for Th1 cell differentiation. Several studies have also shown the role of STAT1 as a tumor suppressor in breast cancer, which is the most common intrusive malignancy and the second most common cause of cancer death in women. Herein, we review the intricate STAT1-mediated molecular mechanisms associated with Th cell differentiation and anti-tumor function in breast cancer.