No abstract

Emerging new and intriguing roles of cytoglobin (Cygb) have attracted considerable attention of cancer researchers in recent years. Hypoxic upregulation of Cygb as well as its altered expression in various human cancers suggest another possible role of this newly discovered globin in tumor cell response under low oxygen tension. Since tumor hypoxia is strongly associated with malignant progression of disease and poor treatment response, it constitutes an area of paramount importance for rational design of cancer selective therapies. However, the mechanisms involved during this process are still elusive. This review outlines the current understanding of Cygb's involvement in tumor hypoxia and discusses its role in tumorigenesis. A better perception of Cygb in tumor hypoxia response is likely to open novel perspectives for future tumor therapy.

Iron metabolism and homeostasis are imperative for the maintenance of normal physiological activities due to the element's critical involvement in a wide variety of crucial biological processes like cellular respiration, metabolic pathways, DNA replication, repair, detoxification, neurotransmission and cellular signaling. Being a key contributor of crucial machineries regulating cellular proliferation and survival, it facilitates the process of tumor growth and development. Thus, tumor cells strive to acquire higher amount of iron than non-malignant cells to satisfy their elevated rate of metabolism. Perhaps, not surprisingly chelation of this metal ion was thought to be effective in treating cancer, but due to a variety of side effects, the use of iron chelators was clinically insignificant. However, discovery of various new classes of iron chelators with lesser side effects and selective toxicity towards cancer cells has revived the possibilities of using iron chelators in anti-cancer therapy. In this review, we have discussed the role of iron in promoting malignant mechanisms and the prospects of usage of different classes of iron chelators in cancer therapeutics.