The Role of Apoptosis as a Double-Edge Sword in Cancer

Abstract

The pathogenesis of many diseases is most closely related to inappropriate apoptosis (either too little or too much) and cancer is one of the situations where too little apoptosis happens, leading to malignant cells that highly proliferate. Defects at any points along apoptotic pathways may lead to malignant transformation of the affected cells, tumor metastasis, and resistance to anti-cancer drugs. Several major molecular mechanisms are involved in the evasion of apoptosis in cancer initiation and progression. Bcl-2 family of proteins and caspases are the central players in the apoptotic mechanism and regulate cell death. Their imperfections cause to the deficient apoptotic signaling and thereby the inadequate apoptosis in cancer cells and eventually carcinogenesis. Strategies targeting these master regulators in carcinoma cells has been a major focus of interest in cancer studies. Therefore, despite being the cause of problem, apoptosis can be targeted in cancer therapy. This chapter provides a comprehensive review of apoptotic cell death and how deficiencies in apoptotic master regulators, caspases and Bcl-2 family proteins, influence carcinogenesis and can be targeted in cancer treatment.

Curcumin nanocapsules effect in apoptotic processes, gene expression, and cell cycle on Hep-G2 cell lines

“…This parallels a recent publication stating CNPs triggered cell death via p53's direct mediation. 8 As mentioned in the research, cancer develops by inhibiting cell death and uncontrolled cell proliferation. That is due to the resistance of tumor cells to apoptosis and to survive and metastasize.…”

“… 7 Dysregulation of apoptosis and growth factor abnormalities cause cancer. 8 Hepatocellular carcinoma (HCC) is one of the most familiar diseases in the world, the third leading cause of cancer-related death, and accounts for more than 80,000 fatalities annually. 9 Several potential drugs were used as promising therapeutic targets for HCC, with varying degrees of inhibition of HCC.…”

Correlation of Some Apoptotic Markers with Chronic Myelogenous Leukemia in Iraqi Patients

“…Their flaws result in insufficient apoptotic signaling, insufficient apoptosis in cancer cells, and ultimately carcinogenesis. As a result, even though it is the root of the issue, apoptosis can be addressed in cancer treatment (35) . Development of novel drugs that render apoptosis-deficient cells susceptible to apoptosis is greatly facilitated by a profound comprehension of the signaling-processes, specific individual players, and apoptosis-related genes.…”

The Reticulon-4 3-bp Deletion/Insertion Polymorphism Is Associated with Structural mRNA Changes and the Risk of Breast Cancer: A Population-Based Case–Control Study with Bioinformatics Analysis

“…Conversely, their decreased expression in cancer cells might lead to apoptosis evasion [15][16][17][18]. Dysregulation between pro-apoptotic and anti-apoptotic proteins is a fundamental element in tumorigenesis, and therefore, any distortions in the expression of RTN4/Nogo, as pro-apoptotic proteins, may increase the susceptibility to cancer, including BC [75,76]. Several mechanisms for the pro-apoptotic activity of Nogo isoforms have been so far described: inducing ER stress and signaling pathways, expressing survivin, interacting with anti-apoptotic proteins such as the Bcl-xL-Bcl-2 family and c-FLIP, and interacting with the JNK-c-Jun MAPK signaling pathways [15][16][17][18]51].…”