Is cancer stimulated by apoptosis?
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Open access•Journal Article 53 Citations | As anticancer agents at low and high concentrations cause apoptosis and necrosis, respectively, cancer cells may be merely injured by an anticancer agent in apoptosis, and cell death may result from an activation of the internal constituents to induce apoptosis. |
| Consequently, in order for cancer to develop and progress, apoptosis must be inhibited. | |
Open access•Journal Article 37 Citations | Apoptosis may be an important mechanism by which cancer cells are killed by certain agents. |
43 Citations | This apoptosis pathway is activated in a cell type-specific manner that is defective in cancer cells, suggesting that this pathway may be targeted during cancer development. |
| Histological examination of treated tumors demonstrated that the treatment-induced mechanism of cancer cell death was by apoptosis. | |
45 Citations | All of these findings cooperate in order to induce apoptosis in cancer cells. |
Open access•Journal Article | Evidence is consistent with the involvement of apoptosis in the cancer-inhibitory activity observed. |
| The abundance of literature suggests that targeting apoptosis in cancer is feasible. | |
38 Citations | Importantly, these mechanisms may also be co-opted by cancer cells in order to evade apoptosis. |
37 Citations | Thus, apoptosis is an attractive target in cancer therapy, with the aim to revert the cancer-related alterations of the cell death machinery. |
Related Questions
How apoptosis affects lung cancer?5 answersApoptosis, or programmed cell death, plays a crucial role in lung cancer. Abnormal regulation of apoptosis can lead to the development and progression of lung tumors. Several signaling pathways, such as NF-κB, PI3K/AKT, and MAPK, are involved in the regulation of apoptosis in lung cancer. MicroRNAs (miRNAs) and their target genes also play a significant role in apoptosis. MiR-146b, 146a, 21, 23a, 135a, 30a, 202, and 181 have been identified as key miRNAs involved in the apoptotic pathway, while IRAK1, TRAF6, Bcl-2, PTEN, Akt, PIK3, KRAS, and MAPK1 are classified as their target genes. Additionally, inhibitors of apoptosis, such as surviving, living, BRUCE, and XIAP, regulate apoptosis by controlling the expression of apoptosis-related genes and miRNAs. Understanding the mechanisms of apoptosis, including signaling pathways, miRNAs/target genes, and inhibitors, can provide valuable insights for the diagnosis, treatment, and prediction of drug response in lung cancer patients.
Apoptosis and Breast Cancer?5 answersApoptosis, or programmed cell death, plays a critical role in breast cancer. It is involved in mammary gland development, differentiation, and function, and its dysregulation contributes to the development and progression of breast cancer. Studies have shown that apoptosis is influenced by various factors, including BRCA and p53 mutations, hormones, and growth factors. The level of apoptosis in breast cancer is associated with clinicopathological variables such as tumor size, ER status, proliferative activity, and p53 expression. High levels of apoptosis are linked to aggressive tumor behavior and poor prognosis. Additionally, apoptosis is related to histological features of breast cancer, such as high grade, lack of tubule formation, and dense infiltration of lymphocytes. Understanding the role of apoptosis in breast cancer can lead to improved diagnosis, treatment, and prediction of disease outcome.
What is the mechanism of apoptosis induced regeneration?5 answersApoptosis-induced regeneration is a process where apoptosis, or programmed cell death, triggers the proliferation of neighboring surviving cells to replace the dying cells. This mechanism is essential for tissue repair and regeneration. Apoptosis acts as a signal to stimulate proliferation within the regenerative tissues, producing the cells needed for full regeneration. In the context of regeneration following necrosis, a form of unregulated cell death, necrosis-induced apoptosis (NiA) occurs independent of changes at the wound edge and does not rely on JNK signaling. Blocking NiA inhibits blastema formation and limits regeneration, suggesting that tissues damaged by necrosis activate programmed cell death at a distance from the injury to promote regeneration. Apoptotic caspases, the effectors of apoptosis, can also mediate the generation of reactive oxygen species (ROS) to promote apoptosis-induced compensatory proliferation (AiP). Apoptosis-induced proliferation is critical for stem cell activity and tissue regeneration, and its dysregulation may contribute to certain forms of cancer.
What are the roles of caspases in radiation-induced apoptosis?4 answersCaspases, specifically caspase 3 and caspase 7, have been found to play roles in radiation-induced apoptosis. Activation of caspase 3 has been shown to attenuate antitumor immune responses induced by radiation therapy (RT) by inhibiting the release of cytosolic DNA. Additionally, sublethal activation of caspase 3 and caspase 7 promotes genetic instability and carcinogenesis, contrary to their perceived roles as tumor suppressors. Furthermore, caspases, including caspase 3, can be activated during apoptosis without executing the cell death program, indicating the existence of caspase-independent cell death pathways despite caspase activation. These findings suggest that caspases, particularly caspase 3, have complex roles in radiation-induced apoptosis, including modulation of immune responses, promotion of genetic instability, and involvement in caspase-independent cell death pathways.
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