Caffeic acid attenuates the angiogenic function of hepatocellular carcinoma cells via reduction in JNK-1-mediated HIF-1α stabilization in hypoxia

RSC Advances ◽  
2016 ◽  
Vol 6 (86) ◽  
pp. 82774-82782 ◽  
Author(s):  
Weiting Gu ◽  
Ye Yang ◽  
Chi Zhang ◽  
Yujia Zhang ◽  
Lijun Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Caffeic Acid ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Hcc Cells

Our study revealed a novel mechanism in the CaA-attenuated angiogenic ability in HCC cells possiblyviareducing the JNK-1-mediated HIF-1α stabilization and inducing the ubiquitination-mediated HIF1α degradation.

scholarly journals MiR-718 mediates the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells

2019 ◽  
Vol 51 (10) ◽  
pp. 500-505 ◽  
Author(s):  
Yuchuan Zhong ◽  
Yan Li ◽  
Tao Song ◽  
Dapeng Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Gastric Cardia Adenocarcinoma ◽  
Indirect Interaction ◽  
Poor Survival ◽  
Hepatocellular Carcinoma Cells ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
B Virus ◽  
Hcc Cells

It has been reported that SEMA3B-AS1 is a tumor-suppressive lncRNA in gastric cardia adenocarcinoma. We explored the possible involvement of SEMA3B-AS1 in hepatocellular carcinoma (HCC). We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In addition, SEMA3B-AS1 expression was not affect by cancer development, and low SEMA3B-AS1 levels were closely correlated with poor survival. SEMA3B-AS1 in HCC tissues was inversely correlated with microRNA (miR)-718 and positively correlated with PTEN. In HCC cells, SEMA3B-AS1 overexpression resulted in upregulated, while miR-718 overexpression resulted in downregulated phosphatase and tensin homolog (PTEN) expression. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells, while miR-718 overexpression resulted in an increased rate. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.

Highly fluorescent QD probes labeling hepatocellular carcinoma cells

RSC Advances ◽  
2015 ◽  
Vol 5 (3) ◽  
pp. 1841-1845 ◽  
Author(s):  
Baiqi Wang ◽  
Hetao Chen ◽  
Rui Yang ◽  
Fang Wang ◽  
Ping Zhou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Liver Cancer Cells ◽  
Hcc Cells

The red signals from the cytoplasm of HCC cells reveal that the QD probes can specifically label liver cancer cells.

scholarly journals Notch1 Signaling Sensitizes Tumor Necrosis Factor-related Apoptosis-inducing Ligand-induced Apoptosis in Human Hepatocellular Carcinoma Cells by Inhibiting Akt/Hdm2-mediated p53 Degradation and Up-regulating p53-dependent DR5 Expression

2009 ◽  
Vol 284 (24) ◽  
pp. 16183-16190 ◽  
Author(s):  
Chunmei Wang ◽  
Runzi Qi ◽  
Nan Li ◽  
Zhengxin Wang ◽  
Huazhang An ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Necrosis Factor ◽  
Notch Signaling ◽  
Tumor Necrosis ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Notch1 Signaling ◽  
Induced Apoptosis ◽  
Necrosis Factor ◽  
Hcc Cells

Notch signaling plays a critical role in regulating cell proliferation, differentiation, and apoptosis. Our previous study showed that overexpression of Notch1 could inhibit human hepatocellular carcinoma (HCC) cell growth by arresting the cell cycle and inducing apoptosis. HCC cells are resistant to apoptotic induction by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), so new therapeutic approaches have been explored to sensitize HCC cells to TRAIL-induced apoptosis. We are wondering whether and how Notch1 signaling can enhance the sensitivity of HCC cells to TRAIL-induced apoptosis. In this study, we found that overexpression of ICN, the constitutive activated form of Notch1, up-regulated p53 protein expression in HCC cells by inhibiting proteasome degradation. p53 up-regulation was further observed in human primary hepatocellular carcinoma cells after activation of Notch signaling. Inhibition of the Akt/Hdm2 pathway by Notch1 signaling was responsible for the suppression of p53 proteasomal degradation, thus contributing to the Notch1 signaling-mediated up-regulation of p53 expression. Accordingly, Notch1 signaling could make HCC cells more sensitive to TRAIL-induced apoptosis, whereas Notch1 signaling lost the synergistic promotion of TRAIL-induced apoptosis in p53-silenced HepG2 HCC cells and p53-defective Hep3B HCC cells. The data suggest that enhancement of TRAIL-induced apoptosis by Notch1 signaling is dependent upon p53 up-regulation. Furthermore, Notch1 signaling could enhance DR5 expression in a p53-dependent manner. Taken together, Notch1 signaling sensitizes TRAIL-induced apoptosis in HCC cells by inhibiting Akt/Hdm2-mediated p53 degradation and up-regulating p53-dependent DR5 expression. Thus, our results suggest that activation of Notch1 signaling may be a promising approach to improve the therapeutic efficacy of TRAIL-resistant HCC.

Oral administration of EGCG solution equivalent to daily achievable dosages of regular tea drinkers effectively suppresses miR483-3p induced metastasis of hepatocellular carcinoma cells in mice

2021 ◽  
Author(s):  
Qingzheng Kang ◽  
Yin Tong ◽  
Vemana Gowd ◽  
Mingfu Wang ◽  
Feng Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Oral Administration ◽  
Carcinoma Cells ◽  
Human Hepatocellular Carcinoma ◽  
Hepatocellular Carcinoma Cells ◽  
Hcc Cells

The effect of non-cytotoxic doses of epigallocatechin-3-gallate (EGCG) on the metastatic capability of human hepatocellular carcinoma (HCC) cells was investigated in vitro and in vivo. miR483-3p, a microRNA whose expression...

Selective toxicity of caffeic acid in hepatocellular carcinoma cells

2018 ◽  
Vol 505 (2) ◽  
pp. 612-617 ◽  
Author(s):  
David L. Brautigan ◽  
Mateusz Gielata ◽  
Jinho Heo ◽  
Ewa Kubicka ◽  
Luke R. Wilkins
Keyword(s):  
Hepatocellular Carcinoma ◽  
Caffeic Acid ◽  
Carcinoma Cells ◽  
Selective Toxicity ◽  
Hepatocellular Carcinoma Cells

scholarly journals P300-dependent acetylation of histone H3 is required for EGFR-mediated HMGA2 transcription in hepatocellular carcinoma

2020 ◽  
Author(s):  
Chao Liang ◽  
Jie Niu ◽  
Xiao Wang ◽  
Xin Yao ◽  
Ruo-Han Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Metastasis ◽  
Histone H3 ◽  
High Mobility ◽  
Carcinoma Cells ◽  
High Mobility Group Protein ◽  
Hepatocellular Carcinoma Cells ◽  
Expression Levels ◽  
Tumor Tissues ◽  
Hcc Cells

Abstract Background High-mobility group protein A2 (HMGA2) is highly expressed in hepatocellular carcinoma cells and contributes to tumor metastasis and poor patient survival. However, the molecular mechanism of HMGA2 transcriptional regulation in hepatocellular carcinoma cells remains largely unclear. Methods Mouse model of lung metastasis was used to evaluate the effects of HMGA2 on hepatocellular carcinoma. DEN-induced rat model of hepatocellular carcinoma was used to measure the expression of HMGA2 and histone H3 acetylation. Immunohistochemistry was used to analyze the expression levels of HMGA2 in 39 matched HCC tissues and adjacent non-tumor tissues. Real-time PCR, Western blotting and Chromatin Immunoprecipitation assay were used to investigate the underlying mechanisms by which HMGA2 overexpression in hepatocellular carcinoma cells. Result Compared with adjacent non-tumour tissues, the expression of HMGA2 was significantly upregulated in human HCC tumor tissues. Moreover, We demonstrated that the expression HMGA2 was upregulated in HCC, and the elevated HMGA2 could promote tumor metastasis. Incubation HCC cells with Epidermal growth factor (EGF) could promote the expression of HMGA2 mRNA and protein. Knockdown of p300 can reverse EGF-induced HMGA2 expression and histone H3-K9 acetylation, while a phosphorylation-mimic p300 S1834D mutant can stimulate HMGA2 expression as well as H3-K9 acetylation in HCC cells. Furthermore, we identified p300-mediated H3-K9 acetylation participates in EGF-induced HMGA2 expression in HCC. In addition, the levels of H3-K9 acetylation positively correlated with the expression levels of HMGA2 in human HCC specimens. Conclusion p300-dependent acetylation of histone H3 is required for EGFR-mediated HMGA2 transcription in hepatocellular carcinoma.

Delivery of microRNA-21-sponge and pre-microRNA-122 by MS2 virus-like particles to therapeutically target hepatocellular carcinoma cells

2021 ◽  
pp. 153537022110356
Author(s):  
Jiawei Zhang ◽  
Dandan Li ◽  
Rui Zhang ◽  
Rongxue Peng ◽  
Jinming Li
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Hepatocellular Carcinoma Cells ◽  
Virus Like Particles ◽  
Invasion And Migration ◽  
Mrna Targets ◽  
And Migration ◽  
Microrna Dysregulation ◽  
Hcc Cells

MicroRNAs are related to the development of hepatocellular carcinoma and can serve as potential therapeutic targets. Therapeutic strategies increasing tumor-suppressive microRNAs and reducing oncogenic microRNAs have been developed. Herein, the effects of simultaneously altering two microRNAs using MS2 virus-like particles were studied. The sequences of microRNA-21-sponge and pre-microRNA-122 were connected and cloned into a virus-like particle expression vector. Virus-like particles containing microRNA-21-sponge and pre-microRNA-122 sequences were prepared and crosslinked with a cell-specific peptide targeting hepatocellular carcinoma cells. Delivery effects were studied using RT-qPCR and functional assays to investigate the level of target mRNAs, cell toxicity, and the effects of proliferation, invasion, and migration. Virus-like particles delivered miR-21-sponge into cells, with the Ct value reaching 10 at most. The linked pre-miR-122 was processed into mature miR-122. The mRNA targets of miR-21 were derepressed as predicted and upregulated 1.2–2.8-fold, and the expression of proteins was elevated correspondingly. Proliferation, migration, and invasion of HCC cells were inhibited by miR-21-sponge. Simultaneous delivery of miR-21-sponge and miR-122 further decreased proliferation, migration, and invasion by up to 34%, 63%, and 65%, respectively. And the combination promoted the apoptosis of HCC cells. In conclusion, delivering miR-21-sponge and miR-122 using virus-like particles modified by cell-specific peptides is an effective and convenient strategy to correct microRNA dysregulation in hepatocellular carcinoma cells and is a promising therapeutic strategy for hepatocellular carcinoma.

HIV-TAT-fused FHIT protein functions as a potential pro-apoptotic molecule in hepatocellular carcinoma cells

2012 ◽  
Vol 32 (3) ◽  
pp. 271-279 ◽  
Author(s):  
Gui-Rong Yu ◽  
Wei-Wei Qin ◽  
Ji-Peng Li ◽  
Wei Hua ◽  
Yan-Ling Meng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Cells ◽  
Large Fraction ◽  
Critical Role ◽  
Carcinoma Cells ◽  
Mechanistic Study ◽  
Hepatocellular Carcinoma Cells ◽  
Hiv Tat ◽  
Fhit Protein ◽  
Hcc Cells

Accumulating evidence has demonstrated that FHIT (fragile histidine triad) is a bona fide tumour suppressor gene in a large fraction of human tumours, including hepatocellular cancer. A virus-based delivery system has been developed to transfer the FHIT gene into many types of cancer cells to inhibit growth or even induce apoptosis. However, a protein-based replacement strategy for FHIT has not been performed in cancer cells. Here, we used HIV-TAT (transactivator of transcription)-derived peptide to transfer the purified FHIT protein into HCC (hepatocellular carcinoma) cells and determine the biological effect of this fusion protein in inducing apoptosis. Affinity chromatography was used to purify TAT peptide-fused human FHIT (TAT–FHIT) protein from BL21 Escherichia coli. Immunofluorescence staining and Western blot analysis were performed to identify the expression and internalization of TAT–FHIT in HCC cells compared with the purified FHIT protein. Our study showed that TAT–FHIT protein can translocate into cancer cells in 1 h after incubation at 37°C. Furthermore, the results of MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] assay, Annexin-V staining and Western blotting demonstrated that TAT–FHIT can robustly inhibit growth and induce apoptosis of HCC cells in vitro. In addition, a mechanistic study showed that both exogenous and intrinsic apoptotic pathways were involved in TAT–FHIT-mediated apoptosis and this effect could be attenuated partially by a mitochondrial protector TAT-BH4, indicating that mitochondrion plays a critical role in TAT–FHIT-mediated pro-apoptotic effect in cancer cells. Taken together, our study suggests that TAT–FHIT is a potential pro-apoptotic molecule in HCC cells and strengthen the hypothesis of its therapeutic application against HCC.

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