Exploring the prognosis of calponin h1 in carcinogenesis: A novel target in biomedical research

Abstract

Calponin h1 serves as a dual-impact factor in the transition from a healthy to an unhealthy state by initiating the progression of cancer onset to its spread. It was initially identified as a protein in smooth muscle, where it interacts with F-actin and inhibits actomyosin Mg-ATPase activity in vitro, regulating smooth muscle contraction. One of its functions is akin to a striated muscle troponin T-like protein. Vertebrate species possess three distinct isoforms of calponin, encoded by the homologous genes CNN1, CNN2, and CNN3, whose structures and genes are elucidated in the subsequent review. Calponin plays varied roles in different types of cancer, such as stomach adenocarcinoma, bladder, colorectal, oral malignancies, fibrosarcoma, lung squamous cell carcinoma, breast and leiomyosarcoma. Its functions may also vary in terms of tissue specificity and varying expression levels. H1 calponin is primarily involved in maintaining blood vessel integrity and controlling smooth muscle contraction, in the cytoskeleton. Stromal myofibroblasts play a crucial role in tumor invasion and metastasis by their capacity to alter the extracellular matrix. Consequently, variations in its expression levels in different malignancies are elucidated, along with an exploration of the associated genetic pathways, by shedding light on their potential impact on prognosis in malignancies.

Keywords

• H1 calponin
• Extracellular matrix
• Stromal myofibroblasts
• Smooth muscle actin