scholarly journals Study on the Mechanism of CircDUSP16 Regulating the Proliferation and Apoptosis of Hepatocarcinoma Cells

2021 ◽  
Author(s):  
Xiaofei Tang ◽  
Yang Xiang
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Ectopic Expression ◽  
Luciferase Gene ◽  
Tissue Samples ◽  
Liver Cancer Cells ◽  
Proliferation And Apoptosis ◽  
Hepatocarcinoma Cells ◽  
The Relationship ◽  
Hcc Cells

Abstract Purpose: This study aims to explore the expression of circDUSP16 in liver cancer and its effect on the proliferation and apoptosis of liver cancer cells. Methods: Real-timePCR was used to measure the expression of circDUSP16, miR-136-5p, and YAP1 in HCC tissues and cells. MTT, colony analysis, and apoptosis analysis were performed to determine the progress of HCC cells. The relationship between circDUSP16, miR-136-5p, and YAP1 was verified by using the luciferase gene experiment. Results: The expression level of circDUSP16 in HCC tissue samples was significantly increased and can be used as an independent prognostic factor for the survival of HCC patients. Inhibition of circDUSP16 can inhibit HCC cell viability, colony formation, and invasion potential. Furthermore, inhibition of circDUSP16 can regulate the expression of YAP1 in the Hippo/YAP signaling pathway in HCC by targeting miR-136-5p, thereby affecting cell proliferation and apoptosis, and participating in the progression of HCC disease. Conclusion: The ectopic expression of circDUSP16 can regulate the expression of YAP1 by competitively binding to miR-136-5p, therefore participating in the progression of HCC, which can provide a new therapeutic target for the treatment of HCC.

scholarly journals TUG1 Promotes the Expression of IFITM3 in Hepatocellular Carcinoma by Competitively Binding to miR-29a

2020 ◽  
Author(s):  
Qian Feng ◽  
Weiwei Liu ◽  
Wenjun Liao ◽  
Jun Gao ◽  
Jiyuan Ai ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Human Liver ◽  
Target Gene ◽  
Liver Cancer Cells ◽  
Tumor Tissues ◽  
Hcc Cells

Abstract Background: Numerous studies have demonstrated the important relationship of TUG1 with tumorigenesis. The present study investigated the role of TUG1 and its downstream genes miR-29a and IFITM3 in the occurrence and development of hepatocellular carcinoma (HCC). We found that both TUG1 and IFITM3 genes are highly expressed in HCC, whereas the expression of miR-29a is low in HCC. Downregulation of TUG1 reduces cell invasion, metastasis, and cell proliferation ability and promotes cell apoptosis. Simultaneous downregulation of miR-29a reverses this effect. Moreover, IFITM3, as the target gene of miR-29a, is positively regulated by TUG1. However, the adjustment relationship between these three components is still unknown and thus warrants further investigation. The present study investigated the regulatory relationship between TUG1, miR-29a, and IFITM3 in human liver cancer.Methods: The expression of TUG1 and miR-29a in tumor tissues and adjacent non-tumor tissues of 65 patients with HCC was detected by real-time quantitative polymerase chain reaction (RT-qPCR). The migration and invasion of liver cancer cells were studied by the wound healing assay and the Transwell method, respectively. The apoptosis rate of HCC cells was detected by flow cytometry, and the proliferation rate of hepatoma cells was detected by the 5-ethynyl-2′-deoxyuridine (EDU) method. Immunofluorescence was used to detect the expression of TUG1 and IFITM3 in HCC-LM3 and HL-7702 cell lines. The relationship between TUG1 and miR-29a was detected using a double luciferase reporter assay and fluorescence in situ hybridization (FISH). Tumors were established in vivo by subcutaneous injection of HCC cells into nude mice and injection of these cells into the tail vein. Western blotting was used to quantify the biomarkers.Results: The expression of TUG1 increased significantly in tumor tissues and HCC cells. Moreover, the expression of miR-29a in liver cancer tissues was significantly lower than that in normal human liver tissues. The expression of TUG1 in liver cancer tissue was negatively correlated with miR-29a. Knockdown of TUG1 weakened the invasion, migration, and proliferation of HCC cells, and enhanced their apoptosis. A simultaneous knockdown of miR-29a enhanced cell invasion, metastasis, and cell proliferation, whereas the apoptosis ability decreased. As a target gene of miR-29a, IFITM3 is not only negatively regulated by miR-29a, but also positively regulated by TUG1. Therefore, TUG1 regulates IFITM3 in HCC cells by competitively binding to miR-29a, thus affecting cell invasion, migration, proliferation, and apoptosis.Conclusion: As a CeRNA, TUG1 competitively binds to miR-29a to regulate IFITM3 and promote the development of liver cancer. Downregulation of TUG1 can significantly inhibit the migration, invasion, and proliferation of liver cancer cells. Based on these results, we conclude that TUG1 could serve as a key gene to improve the prognosis of patients with HCC.

Apatinib regulates the cell proliferation and apoptosis of liver cancer by regulation of VEGFR2/STAT3 signaling

2019 ◽  
Vol 215 (4) ◽  
pp. 816-821 ◽  
Author(s):  
Song Wen ◽  
Guoliang Shao ◽  
Jiaping Zheng ◽  
Hui Zeng ◽  
Jun Luo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Stat3 Signaling ◽  
Proliferation And Apoptosis

scholarly journals MicroRNA-1271 modulates hepatitis B virus replication, cell proliferation and apoptosis in hepatitis B virus-related hepatocellular carcinoma by targeting SIRT1

RSC Advances ◽  
2019 ◽  
Vol 9 (68) ◽  
pp. 39904-39913
Author(s):  
Fei Tang ◽  
Fengmei Wang ◽  
Hongmin Lv ◽  
Huiling Xiang ◽  
Yi Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Virus Replication ◽  
B Virus ◽  
Proliferation And Apoptosis ◽  
Hcc Cells

MiR-1271 suppressed HBV-related HCC cells development by downregulating SIRT1.

scholarly journals Lentivirus-Mediated siRNA Targeting ER-αInhibits Tumorigenesis and Induces Apoptosis in Hepatocarcinoma Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Ping Jiang ◽  
Jun Cao ◽  
Wen-Hui Bai
Keyword(s):  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Dependent Manner ◽  
Gene Therapy Approach ◽  
Protein Levels ◽  
Human Liver Cancer ◽  
Hepatocarcinoma Cells ◽  
Interfering Rna ◽  
Hcc Cells

Background and Objectives. Estrogen receptor-α(ER-α) plays important roles in hepatocarcinogenesis. Recent studies have shown that ER-αcould lead to cell cycle progression or inhibition of apoptosis. To better understand the role of ER-α, RNA interference (RNAi) was used to inhibit ER-αexpression in the human hepatocellular carcinoma (HCC) cells.Methods. Lentivirus-mediated ER-αsmall interfering RNA (siRNA) was transfected into HCC cells Hep3B. ER-αexpression was monitored by real-time polymerase chain reaction (PCR) and western blot. Cell proliferation, apoptosis, and invasion were examined by methyl thiazol tetrazolium (MTT), flow cytometry (FCM), and invasion assay, respectively.Results. ER-αsiRNA efficiently downregulated the expression of ER-αin Hep3B cells at both mRNA and protein levels in a time-dependent manner. ER-αsiRNA also inhibited cell proliferation and reduced cell invasion (compared with other groups,P<0.05, resp.). Furthermore, knockdown of ER-αslowed down the cell population at S phase and increased the rate of apoptosis (P<0.05, resp.).Conclusion. ER-αknockdown suppressed the growth of HCC cells. Thus, ER-αmay play a very important role in carcinogenesis of HCC and its knockdown may offer a new potential gene therapy approach for human liver cancer in the future.

The Effect of miR-155 on the Regulation of Hyperplasia of Middle Membrane of Blood Vessel in Rat Hypertension Model

2019 ◽  
Vol 9 (7) ◽  
pp. 982-987
Author(s):  
Xiaoying Wang ◽  
Yanke Hao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Bioinformatics Analysis ◽  
Luciferase Assay ◽  
Ki 67 ◽  
Vsmc Proliferation ◽  
Tunica Media ◽  
Proliferation And Apoptosis ◽  
The Relationship

Vascular smooth muscle cell (VSMC) abnormal proliferation is related to hypertension. P27 can arrest cell cycle and its downregulation is associated with hypertension. miR-155 plays a regulatory role in VSMC proliferation, while its relationship with hypertension is still unclear. Bioinformatics analysis reveals a relationship between p27 mRNA and miR-155. The present study explores miR-155's role in p27 expression, VSMC proliferation and apoptosis, as well as in the pathogenesis of hypertension. Dual luciferase assay verified the relationship between miR-155 and p27. miR155, p27, α-SMA, and Ki-67 expressions in the thoracic aorta media of rat hypertension model were detected. VSMCs were cultured in vitro and grouped into, anti-miR-NC, anti-miR-155, pIRES2-blank, pIRES2-p27, and anti-miR-155 + pIRES2-p27 groups followed by analysis of cell cycle by flow cytometry and cell proliferation by EdU staining. Hypertension rats were randomly divided into antagomir-155 and antagomir-control. Caudal artery systolic and diastolic pressures were measured. miR-155 suppressed p27 expression. miR-155 and Ki-67 expressions were significantly enhanced, while p27 and α-SMA levels were reduced in the tunica media from hypertension rats compared with control. Downregulation of miR-155 and/or upregulation of p27 obviously declined cell proliferation and arrested cell cycle in G1 phase. Antagomir-155 injection significantly decreased systolic and diastolic pressures, elevated p27 and α-SMA expressions in media, and reduced the thickness of tunica media. miR-155 enhances VSMC proliferation via regulating p27. miR-155 enhancement was related to hypertension. miR-155 plays a therapeutic effect in hypertension.

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 Targeting CDC7 potentiates ATR-CHK1 signaling inhibition through induction of DNA replication stress in liver cancer

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Yuchen Guo ◽  
Jun Wang ◽  
Bente Benedict ◽  
Chen Yang ◽  
Frank van Gemert ◽  
...  
Keyword(s):  
Dna Replication ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Synergistic Effects ◽  
Replication Stress ◽  
Mitotic Catastrophe ◽  
Bioinformatics Analyses ◽  
Liver Cancer Cells ◽  
Dna Replication Stress ◽  
Hcc Cells

Abstract Background Liver cancer is one of the most commonly diagnosed cancers and the fourth leading cause of cancer-related death worldwide. Broad-spectrum kinase inhibitors like sorafenib and lenvatinib provide only modest survival benefit to patients with hepatocellular carcinoma (HCC). This study aims to identify novel therapeutic strategies for HCC patients. Methods Integrated bioinformatics analyses and a non-biased CRISPR loss of function genetic screen were performed to identify potential therapeutic targets for HCC cells. Whole-transcriptome sequencing (RNA-Seq) and time-lapse live imaging were performed to explore the mechanisms of the synergy between CDC7 inhibition and ATR or CHK1 inhibitors in HCC cells. Multiple in vitro and in vivo assays were used to validate the synergistic effects. Results Through integrated bioinformatics analyses using the Cancer Dependency Map and the TCGA database, we identified ATR-CHK1 signaling as a therapeutic target for liver cancer. Pharmacological inhibition of ATR or CHK1 leads to robust proliferation inhibition in liver cancer cells having a high basal level of replication stress. For liver cancer cells that are resistant to ATR or CHK1 inhibition, treatment with CDC7 inhibitors induces strong DNA replication stress and consequently such drugs show striking synergy with ATR or CHK1 inhibitors. The synergy between ATR-CHK1 inhibition and CDC7 inhibition probably derives from abnormalities in mitosis inducing mitotic catastrophe. Conclusions Our data highlights the potential of targeting ATR-CHK1 signaling, either alone or in combination with CDC7 inhibition, for the treatment of liver cancer.

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