6-Shogaol Suppresses the Progression of Liver Cancer via the Inactivation of Wnt/β-Catenin Signaling by Regulating TLR4

Liver cancer is a gastrointestinal malignant tumor with high lethality. The prognosis of liver cancer remains poor. Compounds derived from natural products have been confirmed to alleviate the progression of various diseases, including cancers. Additionally, 6-Shogaol has been reported to induce apoptosis in liver cancer cells. However, the mechanism by which 6-shogaol regulates apoptosis in liver cancer cells remains unclear. To investigate the function of 6-shogaol in liver cancer, RT–qPCR and western blotting were used to detect the expression of TLR4 and FOXO3a in liver cancer cells, respectively. The OD value of liver cancer cells was measured using the MTT assay. Flow cytometry was used to measure cell apoptosis. 6-Shogaol inhibited the growth of liver cancer cells. TLR4 and Wnt/[Formula: see text]-catenin were upregulated in liver cancer cells, and FOXO3a was inactivated, but 6-Shogaol reversed the expression of TLR4, Wnt/[Formula: see text]-catenin and FOXO3a in liver cancer cells. Additionally, TLR4 overexpression partially reversed the inhibitory effect of 6-shogaol on the progression of liver cancer cells via Wnt/[Formula: see text]-catenin signaling. Furthermore, the 6-shogaol-induced increase in FOXO3a expression in liver cancer was notably suppressed by TLR4 or Wnt/[Formula: see text]-catenin upregulation. Thus, 6-Shogaol suppresses the progression of liver cancer by mediating Wnt/[Formula: see text]-catenin signaling and is a potential agent for the treatment of liver cancer.

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RETRACTED ARTICLE: Interference of Mucin 1 inhibits the growth of liver cancer cells by inducing mitochondria-mediated and death receptor-mediated cell apoptosis

Tumor Biology ◽

10.1007/s13277-014-2120-9 ◽

2014 ◽

Vol 36 (2) ◽

pp. 559-559 ◽

Cited By ~ 2

Author(s):

Yongzhen Zhai ◽

Deping Ding ◽

Liya Wei ◽

Enjing Chen ◽

Guohe Feng

Keyword(s):

Liver Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Death Receptor ◽

Mucin 1 ◽

Liver Cancer Cells ◽

Retracted Article

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

Gene ◽

10.1016/j.gene.2018.11.099 ◽

2019 ◽

Vol 691 ◽

pp. 106-113 ◽

Cited By ~ 4

Author(s):

Zhaodong Li ◽

Li Rong ◽

Haifeng Lian ◽

Junning Cheng ◽

Xiaoling Wu ◽

...

Keyword(s):

Liver Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Liver Cancer Cells

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Oncoprotein LAMTOR5 activates GLUT1 via upregulating NF-κB in liver cancer

Open Medicine ◽

10.1515/med-2019-0022 ◽

2019 ◽

Vol 14 (1) ◽

pp. 264-270 ◽

Cited By ~ 6

Author(s):

Jing Zhou ◽

Yajun Li ◽

Danhua Li ◽

Zhi Liu ◽

Jie Zhang

Keyword(s):

Liver Cancer ◽

Cancer Cells ◽

Western Blotting ◽

Glucose Transporter ◽

Luciferase Reporter ◽

Pcr Assay ◽

Glucose Transporter 1 ◽

Over Expression ◽

Liver Cancer Cells ◽

Reporter Assays

AbstractObjectiveAccumulating reports reveal that serving as an oncogenic factor LAMTOR5 is involved in the progression of many specific cancers. Glucose transporter 1 (GLUT1) is frequently identified in many cancers. However, it remains unexplored whether GLUT1 plays a role in LAMTOR5-enhanced liver cancer. Here, we aim to decipher the function of LAMTOR5 in the regulation of GLUT1 in liver cancer.MethodsThe effect of LAMTOR5 on GLUT1 was analyzed using Western blotting and RT-PCR assay. Dose-increased over-expression or silencing of LAMTOR5 was performed through transient transfection. LAMTOR5-activated GLUT1 promoter was revealed by luciferase reporter assay. The regulation of GLUT1 by LAMTOR5/NF-κB was examined via Western blotting and luciferase reporter assays.ResultsThe data showed that in liver cancer cells under the administration with dose-increased LAMTOR5, the level of mRNA and protein of GLUT1 was obviously raised. Our data revealed that the activities of GLUT1 promoter were induced by LAMTOR5. Then, we found that the elevation of GLUT 1 mediated by LAMTOR5 slowed when the inhibitor or siRNAs of NF-κB was introduced into the liver cancer cells. Conclusion. LAMTOR5 is responsible for the activation of GLUT1 via transcription factor NF-κB in liver cancer.

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Carbidopa is an activator of aryl hydrocarbon receptor with potential for cancer therapy

Biochemical Journal ◽

10.1042/bcj20170583 ◽

2017 ◽

Vol 474 (20) ◽

pp. 3391-3402 ◽

Cited By ~ 8

Author(s):

Jiro Ogura ◽

Seiji Miyauchi ◽

Kazumi Shimono ◽

Shengping Yang ◽

Sathisha Gonchigar ◽

...

Keyword(s):

Pancreatic Cancer ◽

Liver Cancer ◽

Aryl Hydrocarbon Receptor ◽

Cancer Cells ◽

Inhibitory Effect ◽

Anticancer Effect ◽

Liver Cancer Cells ◽

Aryl Hydrocarbon

Carbidopa is used with l-DOPA (l-3,4-dihydroxyphenylalanine) to treat Parkinson's disease (PD). PD patients exhibit lower incidence of most cancers including pancreatic cancer, but with the notable exception of melanoma. The decreased cancer incidence is not due to l-DOPA; however, the relevance of Carbidopa to this phenomenon has not been investigated. Here, we tested the hypothesis that Carbidopa, independent of l-DOPA, might elicit an anticancer effect. Carbidopa inhibited pancreatic cancer cell proliferation both in vitro and in vivo. Based on structural similarity with phenylhydrazine, an inhibitor of indoleamine-2,3-dioxygenase-1 (IDO1), we predicted that Carbidopa might also inhibit IDO1, thus providing a molecular basis for its anticancer effect. The inhibitory effect was confirmed using human recombinant IDO1. To demonstrate the inhibition in intact cells, AhR (aryl hydrocarbon receptor) activity was monitored as readout for IDO1-mediated generation of the endogenous AhR agonist kynurenine in pancreatic and liver cancer cells. Surprisingly, Carbidopa did not inhibit but instead potentiated AhR signaling, evident from increased CYP1A1 (cytochrome P450 family 1 subfamily A member 1), CYP1A2, and CYP1B1 expression. In pancreatic and liver cancer cells, Carbidopa promoted AhR nuclear localization. AhR antagonists blocked Carbidopa-dependent activation of AhR signaling. The inhibitory effect on pancreatic cancer cells in vitro and in vivo and the activation of AhR occurred at therapeutic concentrations of Carbidopa. Chromatin immunoprecipitation assay further confirmed that Carbidopa promoted AhR binding to its target gene CYP1A1 leading to its induction. We conclude that Carbidopa is an AhR agonist and suppresses pancreatic cancer. Hence, Carbidopa could potentially be re-purposed to treat pancreatic cancer and possibly other cancers as well.

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A Quinone Isolated from the Nest of Vespa simillima and Its Growth-Inhibitory Effect on Rat Liver Cancer Cells

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.31.722 ◽

2008 ◽

Vol 31 (4) ◽

pp. 722-725 ◽

Cited By ~ 4

Author(s):

Yumiko Fujiwara ◽

Makoto Mangetsu ◽

Ping Yang ◽

Hisayoshi Kofujita ◽

Koichi Suzuki ◽

...

Keyword(s):

Liver Cancer ◽

Cancer Cells ◽

Rat Liver ◽

Inhibitory Effect ◽

Growth Inhibitory Effect ◽

Liver Cancer Cells ◽

Growth Inhibitory

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Inhibitory effect and mechanism of mesenchymal stem cells on liver cancer cells

Tumor Biology ◽

10.1007/s13277-013-1165-5 ◽

2013 ◽

Vol 35 (2) ◽

pp. 1239-1250 ◽

Cited By ~ 29

Author(s):

Lingling Hou ◽

Xiaoyu Wang ◽

Yaqiong Zhou ◽

Haibin Ma ◽

Ziling Wang ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Liver Cancer ◽

Cancer Cells ◽

Inhibitory Effect ◽

Liver Cancer Cells

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

Computational and Mathematical Methods in Medicine ◽

10.1155/2021/3334065 ◽

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.

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

Disease Markers ◽

10.1155/2021/2174290 ◽

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.

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