The interaction mechanism between autophagy and apoptosis in colon cancer

Abstract

Autophagy and apoptosis play crucial roles in tumorigenesis. Recent studies have shown that autophagy and apoptosis have a cross-talk relationship in anti-tumor therapy. It is well established that apoptosis is one of the main pathways of tumor cell death. While autophagy can occurs in tumors with opposite function: protective autophagy and lethal autophagy. Protective autophagy can inhibit tumor apoptosis induced by anticancer drugs, while lethal autophagy can induce tumor cell apoptosis in cooperation with anticancer drugs. Hence, autophagy and apoptosis have synergistic and antagonistic effects in tumor. Colorectal cancer is a common malignant tumor with high morbidity and mortality. In recent years, colorectal carcinoma has achieved improved clinical efficacy with drug treatment. Nonetheless, increasing drug-resistance limit the treatment efficacy, highlighting the urgency of exploring the molecular events that drive drug resistance. Researchers have found that autophagy is one of the major factors leading to drug resistance in colon cancer. Therefore, elucidating the interaction between autophagy and apoptosis is helpful to improve the efficacy of anticancer drugs in clinical treatment of colorectal cancer. This review attaches great importance to the relationship between autophagy and apoptosis and related factors in colorectal cancer.

Down-Regulation of an Autophagy-Related Gene SERPINA1 as a Superior Prognosis Biomarker Associates with Relapse and Distant Metastasis in Colon Adenocarcinoma

“… 22 Meanwhile, autophagy in CRC inhibited the tumor. 33 However, Zhang has found that autophagy plays a stimulative role in the development of CRC. 34 Meanwhile, autophagy can occur in tumors with the opposite function: protective autophagy and lethal autophagy.…”

Cryptotanshinone Inhibits the Growth of HCT116 Colorectal Cancer Cells Through Endoplasmic Reticulum Stress-Mediated Autophagy

“…In the current study, CPT exhibited obvious cytotoxicity on both HCT116 and SW620 cells while have no remarkable effects on SW480 cells, suggesting the selectivity of CPT treatment on CRC cells. Apoptosis is known as type I programmed cell death characterized by chromatin condensation, DNA fragmentation, and the formation of apoptotic bodies (Xie et al, 2020). Various pathways initiated by apoptosis lead to the cleavage of caspase-3, which leads to irreversible cell death (Xu et al, 2017;Xie et al, 2020).…”

“…Apoptosis is known as type I programmed cell death characterized by chromatin condensation, DNA fragmentation, and the formation of apoptotic bodies (Xie et al, 2020). Various pathways initiated by apoptosis lead to the cleavage of caspase-3, which leads to irreversible cell death (Xu et al, 2017;Xie et al, 2020). It has been reported by Xu et al that CPT induced the apoptosis in multidrug-resistant human CRC cells SW620 Ad300 (Xu et al, 2017).…”

“…Autophagy is a process related to autophagy-related genes (ATG), which transports endogenous or exogenous cytoplasmic substances to lysosomes for degradation (Mokarram et al, 2019;Zhao et al, 2021). Thecytoplasmic form of LC3 (LC3-I) is conjured with phosphatidylethanolamine (PE) to form the LC3-phosphatidylethanolamine conjugation (LC3-II), which is known as a hallmark of autophagy (Kang et al, 2019;Xie et al, 2020). Beclin-1 plays an important role in autophagy initiation, which not only affects every link of autophagy, but also plays a key role in the regulation of the interaction between autophagy and apoptosis (Kang et al, 2011;Noguchi et al, 2020).…”

Tandem mass tag-based proteomic analysis reveals cathepsin-mediated anti-autophagic and pro-apoptotic effects under proliferative diabetic retinopathy

“…Autophagy is a stringently regulated process in which cellular debris, degenerated organelles, and aged proteins were wrapped by autophagosome and subsequently degraded by fusion of the autophagosome with lysosome [ 22 ]. Furthermore, a delicate balance usually exists between autophagy and apoptosis within the cell [ 23 , 24 ]. Therefore, we hypothesize that the downregulated expression of cathepsin proteins under PDR may reduce autophagic flux and promote apoptosis in the cell.…”