The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex

Chen, Lanmei; Li, Guodong; Peng, Fa; Jie, Xin-ming; Guangzhi, Dongye; Cai, Kedi; Feng, Ruibing; Li, Baojun; Zeng, Qingwang; Lun, Kaiyi; Chen, Jincan; Xu, Bin

doi:10.18632/oncotarget.13032

Cited by 53 publications

(45 citation statements)

References 70 publications

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“…These results indicated that autophagy could activate apoptosis in luteolin treated HCC cells. On the one hand, our result conflicted with certain previous studies that indicated that autophagy could suppress apoptosis in certain physiological process of cancer [34, 35]. On the other hand, our results were supported by other studies that indicated that autophagy could promote apoptosis in certain physiological process of cancer [36, 37].…”

Section: Discussioncontrasting

confidence: 95%

Luteolin Promotes Cell Apoptosis by Inducing Autophagy in Hepatocellular Carcinoma

Cao

Zhang

Cai

et al. 2017

Cell Physiol Biochem

105

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Background/Aims: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is a leading cause of cancer-related death worldwide. Luteolin, a flavonoid from traditional Chinese medicine, shows anti-cancer activity in many cancer cells, including HCC. However, the mechanism underlying the action of luteolin in HCC, especially its role in regulating cell autophagy, remains unclear. In the present study, we investigated the role of luteolin in regulating cell autophagy and the role of autophagy in luteolin-induced apoptosis. Methods: The 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay (MTT) was used to investigate cell viability. Flow cytometry analysis was used to detect the cell cycle and cell apoptosis. Hoechst 33342 staining was used to detect cell apoptosis. Transmission electron microscopy was used to investigate autophagy. qRT-PCR and western blotting were used to detect apoptosis- and autophagy-related mRNAs and proteins. Results: Luteolin reduced the viability of SMMC-7721 cells in a time and dose-dependent manner, and induced significant G0/G1-phase arrest. In addition, the results of flow cytometry analysis and Hoechst 33342 staining showed that luteolin treatment increased the number of apoptotic cells obviously, and the results of qRT-PCR and western blotting showed that luteolin treatment increased caspase 8 and decreased bcl-2 at the mRNA and protein levels. Furthermore, luteolin increased the number of intracellular autophagosomes, promoted LC3B-I conversion to LC3B-II, and increased Beclin 1 expression. Finally, co-treatment with the autophagy inhibitor chloroquine weakened the effects of luteolin on cell apoptosis. Conclusion: Luteolin induced apoptosis in human liver cancer SMMC-7721 cells, partially via autophagy. Thus, luteolin could be used as a regulator of autophagy in HCC treatment.

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Section: Discussioncontrasting

confidence: 95%

Luteolin Promotes Cell Apoptosis by Inducing Autophagy in Hepatocellular Carcinoma

Cao

Zhang

Cai

et al. 2017

Cell Physiol Biochem

105

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“…50,51 MAPK pathway can regulate many cellular processes, cell proliferation, apoptosis and differentiation, 52 which can be modulated by ROS-dependent redox cycling. [53][54][55] Therefore, we speculated that MAPK pathway might be involved in the regulation of 7-KC-induced apoptosis by autophagy. In our study, 7-KC significantly induced activation of MAPK pathway.…”

Section: Discussionmentioning

confidence: 99%

Macrophage autophagy regulates mitochondria‐mediated apoptosis and inhibits necrotic core formation in vulnerable plaques

Xiao

Che

Cai

et al. 2019

J Cellular Molecular Medi

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The vulnerable plaque is a key distinguishing feature of atherosclerotic lesions that can cause acute atherothrombotic vascular disease. This study was designed to explore the effect of autophagy on mitochondria‐mediated macrophage apoptosis and vulnerable plaques. Here, we generated the mouse model of vulnerable carotid plaque in ApoE−/− mice. Application of ApoE−/− mice with rapamycin (an autophagy inducer) inhibited necrotic core formation in vulnerable plaques by decreasing macrophage apoptosis. However, 3‐methyladenine (an autophagy inhibitor) promoted plaque vulnerability through deteriorating these indexes. To further explore the mechanism of autophagy on macrophage apoptosis, we used macrophage apoptosis model in vitro and found that 7‐ketocholesterol (7‐KC, one of the primary oxysterols in oxLDL) caused macrophage apoptosis with concomitant impairment of mitochondria, characterized by the impairment of mitochondrial ultrastructure, cytochrome c release, mitochondrial potential dissipation, mitochondrial fragmentation, excessive ROS generation and both caspase‐9 and caspase‐3 activation. Interestingly, such mitochondrial apoptotic responses were ameliorated by autophagy activator, but exacerbated by autophagy inhibitor. Finally, we found that MAPK‐NF‐κB signalling pathway was involved in autophagy modulation of 7‐KC–induced macrophage apoptosis. So, we provide strong evidence for the potential therapeutic benefit of macrophage autophagy in regulating mitochondria‐mediated apoptosis and inhibiting necrotic core formation in vulnerable plaques.

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“…132 The process of autophagy is regulated by autophagy-related (ATG) proteins and the role of autophagy in cancer is complex and is contextually dependent. 136 For example, autophagy can inhibit or facilitate cell death. The process of necrosis differs from the apoptosis in a number of ways.…”

Section: Cell Death Processmentioning

confidence: 99%

The development of anticancer ruthenium(ii) complexes: from single molecule compounds to nanomaterials

et al. 2017

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Cancer is rapidly becoming the top killer in the world. Most of the FDA approved anticancer drugs are organic molecules, while metallodrugs are very scarce. The advent of first metal based therapeutic agent, cisplatin, launched a new era in the application of transition metal complexes for therapeutic design. Due to their unique and versatile biochemical properties, ruthenium-based compounds have emerged as promising anti-cancer agents that serve as alternatives to cisplatin and its derivertives. The ruthenium(III) complexes have successfully been used in clinical research and their mechanisms of anticancer action have been reported in large volumes over the past few decades. Ruthenium(II) complexes have also attracted significant attention as anticancer candidates; however, only few of them have been reported comprehensively. In this review, we discuss the development of ruthenium(II) complexes as anticancer candidates and biocatalysts, including arene ruthenium complexes, polypyridyl ruthenium complexes, and ruthenium nanomaterial complexes. This review focuses on the likely mechanisms of action of ruthenium(II)-based anticancer drugs and the relationship between their chemical structures and biological properties. This review also highlights the catalytic activity and the photoinduced activation of ruthenium(II) complexes, their targeted delivery, and their activity in nanomaterial systems.

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The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex

Abstract: In the present study, it was found that the ruthenium (II) imidazole

Cited by 53 publications

References 70 publications

Luteolin Promotes Cell Apoptosis by Inducing Autophagy in Hepatocellular Carcinoma

Luteolin Promotes Cell Apoptosis by Inducing Autophagy in Hepatocellular Carcinoma

Macrophage autophagy regulates mitochondria‐mediated apoptosis and inhibits necrotic core formation in vulnerable plaques

The development of anticancer ruthenium(ii) complexes: from single molecule compounds to nanomaterials

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