Oncostatin M as a Multifunctional Regulator of Breast Cancer Progression: Current Insights and Future Therapeutic Avenues

Abstract

Breast cancer (BC) constitutes the most prevalent malignancy globally, with an incidence of approximately 80%–85% for invasive ductal carcinoma (IDC) and 10%–15% for invasive lobular carcinoma (ILC), and a persistently high mortality and morbidity rate. Although IDC and ILC originate from distinct cellular lineages (ductal and lobular epithelial cells, respectively), they frequently develop in the context of hormonal dysregulation and chronic proliferative stimuli. Recent evidence accumulated over the past decade has demonstrated a role for cytokines belonging to the interleukin‐6 (IL‐6) family in the pathogenesis and progression of BC. These cytokines exert their effects via the activator of transcription (JAK/STAT) pathways, activating downstream Janus kinase/signal transducer, and gp130 receptor subunit activation. As a member of the IL‐6 family, Oncostatin M (OSM.) is critically involved in the processes of autoimmune disorders, inflammation, and oncogenesis, particularly in BC. It has been demonstrated that the overexpression of OSM and OSM receptor (OSMR) plays a pivotal role in cancer cell remodeling and promotes cell proliferation, angiogenesis, survival, invasion, and other hallmark features of BC. However, owing to the involvement of multiple signaling pathways, OSM can exert context‐dependent and even contradictory effects in certain cancer types. This review aims to examine the emerging roles of OSM in BC, elucidate its multifunctional role in tumor regulation and progression, and ultimately explore therapeutic strategies developed to modulate this cytokine in the context of BC.