Role of metal complexes in inhibition of cancer growth factors

Abstract

Cancer is characterized by uncontrolled cell growth, representing a hallmark feature marked by sustained proliferation. This heightened proliferative capacity is primarily driven by the influence of growth factors. Scientific evidence suggests that growth factors play a crucial role in augmenting the transcription of specific proto-oncogenes, such as myc and fos. In the context of cancer development, these growth factors can be either produced by the cancer cells themselves or induce normal cells to release them through intricate signaling mechanisms. The functional diversity of growth factors encompasses various actions, but their predominant mode of operation is through the tyrosine kinase receptor pathway. Tyrosine kinase receptors, comprising integral membrane complexes with intrinsic kinase activity in their cytoplasmic domain, play a pivotal role in transducing signals initiated by the binding of specific growth factors (ligands). This binding event triggers the activation of the kinase function within the receptor, resulting in the phosphorylation of downstream targets on tyrosine and serine residues. Subsequently, this phosphorylation event recruits additional molecules into signaling cascades, amplifying the cellular response. Transition metals, such as Copper, Zinc, and Cobalt, integral to biological systems, play pivotal roles in normal physiological functions. However, dysregulation of these essential metals has been implicated in the pathogenesis of various disorders, including cancer. The narrative unfolds by elucidating the critical role of growth factors in cancer cell proliferation. Key growth factors, such as Transforming Growth Factor-β, Tumour Necrosis Factor-α and Insulin-like Growth Factors, are explored within the context of cancer progression. The intricate signaling pathways, particularly the Tyrosine Kinase Receptor pathway, are examined to understand how metal complexes may disrupt these pathways, impeding uncontrolled cell growth. Furthermore, this review provides an in-depth examination of medicinal inorganic chemistry, emphasizing the ability of transition metal complexes to form charged ions and induce hydrolysis reactions. The nuanced discussion underscores the necessity for precise dosages of metal-containing drugs to avoid undesirable toxicity, acknowledging the delicate balance required for optimal therapeutic responses. This comprehensive review delves into metal complexes of Cobalt, Copper, Zinc, and metal nanoparticles as promising inhibitors of cancer growth factors. By explicating the intricate interplay between metal complexes and growth factor pathways, this article contributes to the ongoing scientific exploration of novel and effective anticancer strategies.