Mini Review - Journal of Biotechnology and Phytochemistry (2023) Volume 7, Issue 3

Antiproliferative and cytotoxic effects of cardiac glycosides

Verdick Jacob^*

Department of Biotechnology

*Corresponding Author:

Verdick Jacob
Department of Biotechnolog
Max Planck Institute
Germany
E-mail: vj@mpimp-golm.mpg.de

Received:29-May-2023, Manuscript No. AAJBP-23-101747; Editor assigned:01-Jun-2023, PreQC No. AAJBP-23-101747(PQ); Reviewed:15-Jun-2023, QC No. AAJBP-23-101747; Revised:19-Jun-2023, Manuscript No. AAJBP-23-101747(R); Published:26-Jun-2023, DOI:10.35841/ aajbp-7.3.154

Citation: Jacob V. Antiproliferative and cytotoxic effects of cardiac glycosides. 2023;7(3):154

Abstract

Cardiac glycosides are a class of natural compounds with diverse biological activities, including antiproliferative and cytotoxic effects. This abstract summarizes recent research on the potential therapeutic applications of cardiac glycosides in cancer treatment. Studies have revealed their ability to inhibit cell proliferation and induce cell death in various cancer cell lines. Mechanistically, cardiac glycosides target key signaling pathways involved in cancer progression, such as the Na+/K+-ATPase pump and the Wnt/β-catenin pathway. Moreover, they have shown synergistic effects with conventional chemotherapeutic agents, suggesting their potential use as adjuvants in combination therapies. These findings highlight the promising role of cardiac glycosides as novel anticancer agents and warrant further investigation to unlock their full therapeutic potential

Keywords

Cardiac glycosides, Cell cycle arrest, Cancer cells, Tumor growth

Introduction

Cardiac glycosides are a class of natural compounds that have been traditionally used for the treatment of cardiovascular diseases, particularly congestive heart failure and atrial fibrillation. These compounds, derived from various plant sources, exhibit potent effects on the heart by inhibiting the Na+/K+-ATPase pump and increasing cardiac contractility. However, in recent years, researchers have discovered that cardiac glycosides also possess antiproliferative and cytotoxic properties, making them potential candidates for the development of novel anticancer therapies [1].

The antiproliferative and cytotoxic effects of cardiac glycosides have been investigated in various cancer cell lines, including breast, colon, lung, prostate, and leukemia. Several studies have demonstrated that cardiac glycosides can inhibit cell proliferation and induce cell death in these cancer cells. One of the key mechanisms underlying these effects is the inhibition of the Na+/K+-ATPase pump, which leads to an increase in intracellular calcium levels. Elevated calcium levels activate various signaling pathways, including the calcineurin-NFAT pathway and the PI3K/Akt pathway, which regulate cell survival, proliferation, and apoptosis [2].

Cardiac glycosides have been shown to induce apoptosis, or programmed cell death, in cancer cells. Apoptosis is a highly regulated process that plays a crucial role in maintaining tissue homeostasis and eliminating damaged or abnormal cells. Dysregulation of apoptosis is a hallmark of cancer, and the ability of cardiac glycosides to induce apoptosis in cancer cells makes them attractive candidates for anticancer therapy. Studies have shown that cardiac glycosides can activate apoptotic pathways, such as the caspase cascade, leading to the cleavage of key cellular proteins and ultimately resulting in cell death. In addition to apoptosis, cardiac glycosides can also trigger other forms of cell death, including autophagy and necrosis. Autophagy is a cellular process that involves the degradation and recycling of cellular components to maintain cellular homeostasis. While autophagy can promote cell survival under certain conditions, excessive or prolonged autophagy can lead to cell death. Cardiac glycosides have been shown to induce autophagy in cancer cells, and the interplay between autophagy and apoptosis in response to cardiac glycoside treatment is an area of active research [3].

Furthermore, cardiac glycosides can induce necrosis, a form of cell death characterized by cell swelling, membrane rupture, and the release of intracellular contents. Necrosis is typically associated with inflammation and is considered an uncontrolled form of cell death. The ability of cardiac glycosides to induce necrosis in cancer cells suggests that they can target tumor cells through multiple mechanisms, leading to their elimination. Interestingly, the antiproliferative and cytotoxic effects of cardiac glycosides appear to be selective for cancer cells, sparing normal cells. Several studies have demonstrated that cancer cells are more sensitive to the cytotoxic effects of cardiac glycosides compared to non-cancerous cells. This selective cytotoxicity may be attributed to differences in the expression levels of the Na+/K+-ATPase pump and other factors involved in cardiac glycoside uptake and signaling pathways between cancer and normal cells. This selectivity is advantageous in cancer therapy, as it reduces the potential for off-target effects and toxicity to normal tissues [4].

In addition to their direct effects on cancer cells, cardiac glycosides have also been shown to modulate the tumor microenvironment. The tumor microenvironment plays a critical role in cancer progression and response to therapy. Cardiac glycosides have been reported to inhibit angiogenesis, the process of new blood vessel formation that is essential for tumor growth and metastasis. By inhibiting angiogenesis, cardiac glycosides can limit the blood supply to tumors, thereby depriving them of oxygen and nutrients, and potentially enhancing the efficacy of other anticancer treatments [5].

Conclusion

The discovery of the antiproliferative and cytotoxic effects of cardiac glycosides has opened up new avenues for their potential use in cancer therapy. The ability of cardiac glycosides to induce apoptosis, autophagy, and necrosis in cancer cells, as well as their selectivity towards cancer cells, make them attractive candidates for further research and development.

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