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 Downregulation of PITX2 inhibits the proliferation and migration of liver cancer cells and induces cell apoptosis

2021 ◽  
Vol 16 (1) ◽  
pp. 1322-1329
Author(s):  
Kebinuer Tuerxun ◽  
Shufang Zhang ◽  
Yuexin Zhang
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
And Migration ◽  
Pitx2 Expression

Abstract Paired-like homeodomain 2 (PITX2) functions as a transcription factor to participate in vertebrate embryogenesis, and dysregulated PITX2 expression was associated with the progression of various cancers. The functional role of PITX2 in tumorigenesis of liver cancer remains unknown. Western blot analysis showed that expression levels of PITX2 were enhanced in the liver cancer tissues and cells. siRNAs targeting PITX2 induced downregulation of PITX2 in liver cancer cells. siRNA-induced knockdown of PITX2 decreased liver cancer cell viability and proliferation, while promoting cell apoptosis by increasing cleaved-PARP, cleaved caspase 3, and cleaved caspase 9. The knockdown of PITX2 repressed liver cancer cell migration and invasion. In conclusion, elevated PITX2 expression was associated with liver cancer progression through repression of cell apoptosis and promoting cell proliferation and metastasis, and silencing of PITX2 might serve as a potential therapeutic strategy for the treatment of liver 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 Down-Regulation of SUZ12 Accelerates the Migration and Invasion of Liver Cancer Cells via Activating ERK1/2 Pathway

2019 ◽  
Vol 10 (6) ◽  
pp. 1375-1384 ◽  
Author(s):  
Cailin Xue ◽  
Kunyuan Wang ◽  
Xiaofeng Jiang ◽  
Chengxin Gu ◽  
Ganxiang Yu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Liver Cancer Cells

scholarly journals Downexpression of HSD17B6 correlates with clinical prognosis and tumor immune infiltrates in hepatocellular carcinoma

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Lei Lv ◽  
Yujia Zhao ◽  
Qinqin Wei ◽  
Ye Zhao ◽  
Qiyi Yi
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Immune Responses ◽  
Cancer Cells ◽  
Negative Regulator ◽  
Functional Enrichment ◽  
Migration And Invasion ◽  
Relative Reduction ◽  
Clinical Prognosis ◽  
Liver Cancer Cells

Abstract Background Hydroxysteroid 17-Beta Dehydrogenase 6 (HSD17B6), a key protein involved in synthetizing dihydrotestosterone, is abundant in the liver. Previous studies have suggested a role for dihydrotestosterone in modulating progress of various malignancies, and HSD17B6 dysfunction was associated with lung cancer and prostate cancer. However, little is known about the detailed role of HSD17B6 in hepatocellular carcinoma (HCC). Methods Clinical implication and survival data related to HSD17B6 expression in patients with HCC were obtained through TCGA, ICGC, ONCOMINE, GEO and HPA databases. Survival analysis plots were drawn with Kaplan–Meier Plotter. The ChIP-seq data were obtained from Cistrome DB. Protein–Protein Interaction and gene functional enrichment analyses were performed in STRING database. The correlations between HSD17B6 and tumor immune infiltrates was investigated via TIMER and xCell. The proliferation, migration and invasion of liver cancer cells transfected with HSD17B6 were evaluated by the CCK8 assay, wound healing test and transwell assay respectively. Expression of HSD17B6, TGFB1 and PD-L1 were assessed by quantitative RT-PCR. Results HSD17B6 expression was lower in HCC compared to normal liver and correlated with tumor stage and grade. Lower expression of HSD17B6 was associated with worse OS, PFS, RFS and DSS in HCC patients. HNF4A bound to enhancer and promoter regions of HSD17B6 gene, activating its transcription, and DNA methylation of HSD17B6 promoter negatively controlled the expression. HSD17B6 and its interaction partners were involved in androgen metabolism and biosynthesis in liver. HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infiltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1. Conclusions This study indicate that HSD17B6 could be a new biomarker for the prognosis of HCC and an important negative regulator of immune responses in HCC.

scholarly journals Inhibition of RFX6 Suppresses the Invasive Ability of Tumor Cells Through the Notch Pathway and Affects Tumor Immunity in Hepatocellular Carcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Mu Song ◽  
Mulati Kuerban ◽  
Lu Zhao ◽  
Xiaolin Peng ◽  
Youqin Xu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Immune Cell ◽  
Biological Effects ◽  
Biological Significance ◽  
Notch Pathway ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Liver Hepatocellular Carcinoma

BackgroundThe DNA-binding protein RFX6 was overexpressed in hepatocellular carcinoma, and its expression level was correlated with the prognosis and immune cell infiltration in liver hepatocellular carcinoma. However, the mechanism of the abnormal expression and the biological effects of RFX6 in liver cancer remains unknown.MethodsTo understand the specific expression mechanism of RFX6 in liver cancer, we performed bioinformatic prediction, CHIP-qPCR assay, co-IP, and dual-luciferase assay to assess the regulating mechanism of RFX6. In the meantime, a series of biological experiments in vivo and in vitro were conducted to analyze the biological significance of RFX6 in hepatocellular carcinoma.ResultsWe demonstrated that knockdown of RFX6 in liver cancer cells significantly suppressed the proliferation, migration, and invasion of cancer cells. Moreover, inhibition of RFX6 could affect the immune response of T cells. Among a number of interacting proteins, we revealed that RFX6 directly binds to DTX2, a regulator of the Notch signaling pathway by targeting NOTCH1, and helps in its transcription stability. Furthermore, we discovered that miRNA-542-3p, the expression of which was decreased in hepatocellular carcinoma, was directly involved in the negative regulation of the expression of RFX6.ConclusionIn summary, we discovered that the miRNA-542-3p–RFX6–DTX2–NOTCH1 regulatory pathway played significant roles in the tumor progression of liver hepatocellular carcinoma.

scholarly journals Roles of CXCL5 on migration and invasion of liver cancer cells

2014 ◽  
Vol 12 (1) ◽  
pp. 193 ◽  
Author(s):  
Xiaojing Xu ◽  
Peixin Huang ◽  
Biwei Yang ◽  
Xiangdong Wang ◽  
Jinglin Xia
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Liver Cancer Cells

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.

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