scholarly journals Cu(II) Coordination Polymer Inhibits Liver Cancer Development via Targeting BCL-2 Protein and Activating Apoptotic Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Jing Zhou ◽  
Xiaowen Peng ◽  
Xuejiao Li ◽  
Xiaoyu Kong
Keyword(s):  
Liver Cancer ◽  
Coordination Polymer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Human Cancer ◽  
Solvothermal Reaction ◽  
Ros Generation ◽  
Caspase 9 ◽  
Liver Cancer Cells

In the current study, a Cu(II) coordination polymer (CP) has been created in success with the solvothermal reaction between an asymmetrical rigid N-heterocyclic carboxylatic acid (HL) and Cu(NO3)2·3H2O in the existence of 1,3-H2bdc, the second assistant ligand (in which 1,3-H2bdc is benzene-1,3-dicarboxylic acid and HL is 1-(4-carboxylphenyl)-3-(prazin-2-yl)-1H-1,2,4-triazole), and the chemical composition of this compound is [Cu2(L)2(1,3-bdc)(H2O)2]n (1). In the biological aspect, we screened the antiproliferation activity of the Cu(II) coordination polymer on five kinds of human cancer cell lines. IC50 and MTT assay results indicated that complex 1 had a spectral antiproliferative activity against liver cancer cells, peculiarly on human HepG2 liver cancer cells. From the data of Annexin V-FITC/PI assay and ROS detection, we can find that complex 1 exerts an antitumor effect by inducing ROS generation and cell apoptosis. Caspase-3 and caspase-9 activity detection revealed that activation of caspase-3 and caspase-9 plays vital roles in HepG2 cell apoptosis. These outcomes indicate that 1 is an excellent compound in treating cancer.

Knockdown MTMR14 promotes cell apoptosis and inhibits migration in liver cancer cells

Gene ◽  
2019 ◽  
Vol 691 ◽  
pp. 106-113 ◽  
Author(s):  
Zhaodong Li ◽  
Li Rong ◽  
Haifeng Lian ◽  
Junning Cheng ◽  
Xiaoling Wu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Liver Cancer Cells

scholarly journals The Anti-Tumor Effect and Underlying Apoptotic Mechanism of Ginsenoside Rk1 and Rg5 in Human Liver Cancer Cells

Molecules ◽  
2021 ◽  
Vol 26 (13) ◽  
pp. 3926
Author(s):  
Chen Chen ◽  
Qing Lv ◽  
Yang Li ◽  
Ying-Hua Jin
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Human Cancer ◽  
Mitogen Activated Protein Kinase ◽  
Network Pharmacology ◽  
Signal Pathways ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

Ginsenoside Rk1 and Rg5 are minor ginseng saponins that have received more attention recently because of their high oral bioavailability. Each of them can effectively inhibit the survival and proliferation of human liver cancer cells, but the underlying mechanism remains largely unknown. Network pharmacology and bioinformatics analysis demonstrated that G-Rk1 and G-Rg5 yielded 142 potential targets, and shared 44 putative targets associated with hepatocellular carcinoma. Enrichment analysis of the overlapped genes showed that G-Rk1 and G-Rg5 may induce apoptosis of liver cancer cells through inhibition of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signal pathways. Methyl thiazolyl tetrazolium (MTT) assay was used to confirm the inhibition of cell viability with G-Rk1 or G-Rg5 in highly metastatic human cancer MHCC-97H cells. We evaluated the apoptosis of MHCC-97H cells by using flow cytometry and 4′,6-diamidino-2-phenylindole (DAPI) staining. The translocation of Bax/Bak led to the depolarization of mitochondrial membrane potential and release of cytochrome c and Smac. A sequential activation of caspase-9 and caspase-3 and the cleavage of poly(ADP-ribose) polymerase (PARP) were observed after that. The levels of anti-apoptotic proteins were decreased after treatment of G-Rk1 or G-Rg5 in MHCC-97H cells. Taken together, G-Rk1 and G-Rg5 promoted the endogenous apoptotic pathway in MHCC-97H cells by targeting and regulating some critical liver cancer related genes that are involved in the signal pathways associated with cell survival and proliferation.

scholarly journals miR-18a-5p Targets FBP1 to Promote Proliferation, Migration, and Invasion of Liver Cancer Cells and Inhibit Cell Apoptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Shan Gao ◽  
Dongjie Zhu ◽  
Jian Zhu ◽  
Lianqiang Shen ◽  
Ming Zhu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Malignant Tumors ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Liver Cancer Cells ◽  
Treatment Plans ◽  
New Treatment

Liver cancer is one of the most aggressive malignant tumors. It is significant to understand the molecular mechanism of liver cancer cells to develop new treatment plans. Studies have identified that FBP1 serves as a cancer inhibitor gene. To research the effect mechanism of FBP1 in liver cancer cells, bioinformatics analysis was performed to study its expression in liver cancer tissue. Survival analysis was also performed. Moreover, starBase database was applied to predict upstream regulatory genes of FBP1. Dual-luciferase assay was performed to testify their targeted relationship. The mRNA and protein expression levels of FBP1 in liver cancer cells were detected by qRT-PCR and western blot, respectively. Cell viability was analyzed by CCK-8 assay. The migratory and invasive abilities of cells were analyzed by Transwell assay. The apoptosis of liver cancer cells was detected by flow cytometry. The results showed that the expression of FBP1 was downregulated in liver cancer tissue and cells. FBP1 low expression was correlated with the poor prognosis of patients. miR-18a-5p could inhibit FBP1 expression. Overexpression of FBP1 could inhibit the progression of liver cancer cells and promote cell apoptosis. Overexpressing miR-18a-5p could promote the progression of liver cancer cells and inhibit cell apoptosis. However, overexpressing FBP1 simultaneously could reverse the effect. miR-18a-5p and FBP1 are expected to be candidates for liver cancer treatment.

scholarly journals Amarogentin Induces Apoptosis of Liver Cancer Cells via Upregulation of p53 and Downregulation of Human Telomerase Reverse Transcriptase in Mice

2016 ◽  
Vol 16 (5) ◽  
pp. 546-558 ◽  
Author(s):  
Chun Huang ◽  
Runqin Li ◽  
Yinglin Zhang ◽  
Jianping Gong
Keyword(s):  
Liver Cancer ◽  
Protein Expression ◽  
Reverse Transcriptase ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Telomerase Reverse Transcriptase ◽  
Human Telomerase Reverse Transcriptase ◽  
Liver Cancer Cells ◽  
Gene And Protein Expression ◽  
Human Telomerase

Background and Objective: Amarogentin has been reported to have a preventive effect on liver cancer via inducing cancer cell apoptosis. We attempted to elucidate the roles of p53-associated apoptosis pathways in the chemopreventive mechanism of amarogentin. The findings of this study will facilitate the development of a novel supplementary strategy for the treatment of liver cancer. Materials and Methods: The purity of amarogentin was assessed by high-performance liquid chromatography. The inhibitory ratios of the liver cell lines were determined using a Cell Counting Kit-8 following treatment with a gradient concentration of amarogentin. Cell apoptosis was detected by flow cytometry using annexin V-fluorescein isothiocyanate/propidium iodide kits. The gene and protein expression of p53-associated molecules, such as Akt, human telomerase reverse transcriptase, RelA, and p38, was detected by real-time quantitative polymerase chain reaction, Western blotting, and immunohistochemical staining in liver cancer cells and mouse tumor tissues after treatment with amarogentin. Results: The inhibitory effect of amarogentin on cell proliferation was more obvious in liver cancer cells, and amarogentin was more likely to induce the apoptosis of liver cancer cells than that of normal liver cells. The gene and protein expression levels of Akt, RelA, and human telomerase reverse transcriptase were markedly higher in the control group than in the preventive group and treatment groups. Only the expression of human telomerase reverse transcriptase was downregulated, accompanied by the upregulation of p53. Conclusion: The results of our study suggest that amarogentin promotes apoptosis of liver cancer cells by the upregulation of p53 and downregulation of human telomerase reverse transcriptase and prevents the malignant transformation of these cells.

scholarly journals TRIB2 desensitizes ferroptosis via βTrCP-mediated TFRC ubiquitiantion in liver cancer cells

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Susu Guo ◽  
Yuxin Chen ◽  
Xiangfei Xue ◽  
Yueyue Yang ◽  
Yikun Wang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Adaptor Protein ◽  
Ros Generation ◽  
Iron Level ◽  
E3 Ligases ◽  
Labile Iron Pool ◽  
Liver Cancer Cells ◽  
Labile Iron

AbstractTribbles homolog 2 (TRIB2) is known to boost liver tumorigenesis via regulating Ubiquitin (Ub) proteasome system (UPS). At least two ways are involved, i.e., acts as an adaptor protein to modulate ubiquitination functions of certain ubiquitin E3 ligases (E3s) and reduces global Ub levels via increasing the proteolysis activity of proteasome. Recently, we have identified the role of TRIB2 to relieve oxidative damage via reducing the availability of Ub that is essential for the ubiquitination and subsequent degradation of Glutathione peroxidase 4 (GPX4). Although GPX4 is a critical antioxidant factor to protect against ferroptosis, the exact evidence showing that TRIB2 desensitizes ferroptosis is lacking. Also, whether such function is via E3 remains unclear. Here, we demonstrated that deletion of TRIB2 sensitized ferroptosis via lifting labile iron in liver cancer cells. By contrast, overexpression of TRIB2 led to the opposite outcome. We further demonstrated that transferrin receptor (TFRC) was required for TRIB2 to desensitize the cells to ferroptosis. Without TFRC, the labile iron pool could not be reduced by overexpressing TRIB2. We also found that beta-transducin repeat containing E3 ubiqutin protein ligase (βTrCP) was a genuine E3 for the ubiquitination of TFRC, and TRIB2 was unable to decline labile iron level once upon βTrCP was knocked out. In addition, we confirmed that the opposite effects on ferroptosis and ferroptosis-associated lipid reactive oxygen species (ROS) generation resulted from knockout and overexpression of TRIB2 were all indispensible of TFRC and βTrCP. Finally, we demonstrated that TRIB2 exclusively manipulated RSL3- and erastin-induced-ferroptosis independent of GPX4 and glutathione (GSH). In conclusion, we elucidated a novel role of TRIB2 to desensitize ferroptosis via E3 βTrCP, by which facilitates TFRC ubiquitiation and finally decreases labile iron in liver cancer cells.

scholarly journals Dodecanoic acid induces oxidative stress-mediated apoptotic death in liver cancer cells through mitochondrial pathway

2020 ◽  
Author(s):  
xiaoguang chen ◽  
Liwei Guo ◽  
Yumei Liu ◽  
Xuemin Zhu ◽  
Qiongxia Lv
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Saturated Fatty Acids ◽  
Mitochondrial Pathway ◽  
Dodecanoic Acid ◽  
Atp Content ◽  
Liver Cancer Cells

Abstract Background Dodecanoic acid (DDA), a medium chain saturated fatty acids, has been reported to have anticancer activity in reproductive system cancer and some digestive tract cancers. However, the role and the underlying mechanism of DDA in liver cancer have been rarely defined. Methods Mouse liver cancer Hepa 1–6 cells were administrated with DDA in this present study. Apoptosis, cell cycle analysis, mitochondrial membrane potential (MMP) and ATP content were determined by flow cytometry; GSH availability, ROS level and SOD activity was assessed by a microplate reader; Bcl-2, Bax and Caspase-3 protein levels were analyzed by western blot. Results 0.5 mM DDA was identified as the ideal concentration for investigation and could time-dependently inhibit cell viability. DDA-treated cells had a significant, time-dependent increase in cell apoptotic rate in spite of an accumulation of the cells in S + G2/M phase of the cell cycle. The enhanced level of ROS, depletion of GSH and the reduced activity of SOD in DDA-treated cells indicated the generation of oxidative stress; mitochondrial dysfunction was evidenced by the dissipation of MMP of and the reduction in ATP content. Cell death via mitochondrial pathway was indicated by the reduced Bcl-2/Bax ratio and the increased level of caspase-3 protein. Conclusions Taken together, DDA effectively triggers oxidative stress-induced death in liver cancer cells by disturbing the structure and function of mitochondria. The findings provide an in-depth insight into the potential action mechanism of DDA on liver cancer.

scholarly journals Rhein induces liver cancer cells apoptosis via activating ROS-dependent JNK/Jun/caspase-3 signaling pathway

2020 ◽  
Vol 11 (2) ◽  
pp. 500-507 ◽  
Author(s):  
Aili Wang ◽  
Huihong Jiang ◽  
Yuanyuan Liu ◽  
Jing Chen ◽  
Xue Zhou ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Liver Cancer Cells
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