Upregulated GP73 expression and downregulated NLRP3 expression in liver cancer tissues correlate with patient’s survival

2018 ◽  
Vol 7 (2) ◽  
pp. 441-449
Author(s):  
Yixin Mao ◽  
Huayu Yang ◽  
Lejia Sun ◽  
Yilei Mao ◽  
Xianju Qin
Keyword(s):  
Liver Cancer ◽  
Cancer Tissues ◽  
Nlrp3 Expression

scholarly journals miR-183-5p promotes proliferation and migration in hepatocellular carcinoma by targeting IRS1 and its association with patient survival

2020 ◽  
Vol 35 (3) ◽  
pp. 83-89
Author(s):  
Rong Yan ◽  
Kang Li ◽  
Dawei Yuan ◽  
Haonan Wang ◽  
Wei Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Cancer Progression ◽  
Normal Tissues ◽  
Report Analysis ◽  
In Vitro Effects ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Background: MiR-183-5p plays an important role in the pathophysiology of many tumors, while the role of MiR-183-5p in liver cancer is unclear. Methods: In this study, quantitative reverse transcription-polymerase chain reaction and Western blotting were used to detect the expression of miR-183-5p in liver cancer cell lines, liver cancer tissues, and normal tissues adjacent to the cancer, and to explore the mechanism of miR-183-5p regulating liver cancer progression. The in vitro effects of miR-183-5p were evaluated by CCK-8, colony formation test, and wound healing test. Various databases were used to predict the target mRNA of miR-183-5p and verified by luciferase report analysis. In addition, the effects of miR-183-5p and its target gene on the survival of patients with liver cancer were also analyzed. Results: miR-183-5p was highly expressed in hepatocellular carcinoma cells and tissues, and was related to some clinicopathological features. MiR-183-5p can promote the proliferation and migration of liver cancer cells. Using the bioinformatics database, we proved that miR-183-5p is related to the survival of liver cancer patients. Insulin receptor substrate 1 (IRS1) is a target of miR-183-5p, and luciferase analysis confirmed that miR-183-5p combines with the 3′-untranslated region (3′-UTR) of IRS1. Conclusion: The miR-183-5p/IRS1 axis may be a new target for liver cancer research.

scholarly journals MiR-129-5p inhibits liver cancer growth by targeting calcium calmodulin-dependent protein kinase IV (CAMK4)

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Zhengzhao Li ◽  
Junyu Lu ◽  
Guang Zeng ◽  
Jielong Pang ◽  
Xiaowen Zheng ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Liver Cancer ◽  
Target Gene ◽  
Liver Cells ◽  
Migration And Invasion ◽  
Dependent Protein Kinase ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
Direct Target ◽  
Cancer Tissues

Abstract This study was designed to investigate the mechanism by which miR-129-5p affects the biological function of liver cancer cells. The expression levels of miR-129–5p in liver cancer tissues and cells were, respectively, determined. Crystal violet staining and flow cytometry were used to detect cell proliferation and apoptosis. Wound healing assay and transwell assay were performed to test cell migration and invasion. The target gene of miR-129–5p was analyzed and verified by bioinformatics analysis and luciferase reporter assay. Tumorigenicity assays in nude mice were used to test the antitumor ability of calcium calmodulin-dependent protein kinase IV (CAMK4). miR-129–5p was found to be underexpressed in hepatocellular cancer tissues and cells and also to inhibit liver cells proliferation, migration, and invasion and promote apoptosis. CAMK4 was a direct target for miR-129–5p and was lowly expressed in liver cancer tissues and cells. CAMK4 was also found to inhibit liver cells proliferation, migration and invasion, and promote apoptosis. CAMK4 might exert an antitumor effect by inhibiting the activation of mitogen-activated protein kinase (MAPK). MiR-129–5p was a tumor suppressor with low expression in liver cancer tissues and cells. CAMK4, which is a direct target gene of miR-129–5p, could inhibit tumor by inhibiting the activation of MAPK signaling pathway.

scholarly journals Telocytes Promote the Metastasis of Hepatocellular Carcinoma by Activating ERK Signaling Pathway and Sponging miR-942-3p to Impact MMP9

2021 ◽  
Author(s):  
Ying Xu ◽  
Hu Tian ◽  
Chao Guang Luan ◽  
Kai Sun ◽  
peng Jin Bao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Cancer Tissue ◽  
Proliferative Potential ◽  
Cancer Tissues ◽  
Hcc Cells

Abstract Background: Hepatocellular carcinoma(HCC) in China is considered as a familiar malignant tumor with poor prognosis, high metastasis and disease relapse. Telocytes(TCs) have been verified to participate in progresses of tumorigenesis, invasions and migrations by secreting functional proteins and transmitting cell-to-cell information. Extracellular signal-regulared protein kinase(ERK) signal pathway is a vital mechanism driving cell proliferation, metastasis and apoptosis, but whether this molecular signaling mechanism contributes to matrix metalloproteinase-9(MMP) expression of TCs remains unclear. Methods: Telocytes and MMP9 expression in the liver cancer tissues are measured by immunohistochemistry assay, Westen blot assay and RT-PCR technique, meanwhile primary telocytes from liver para-cancer tissues are cultured in vitro. To demonstrate the function of telocytes for hepatocellular carcinoma, the metastatic cancer animal model is established by three typs of liver cancer cell-lines in vivo. Results: In our study, we elucidate that TCs in the para-cancer tissue can promote the metastasis of HCC cells by MMP-9 expression, in vitro and in vivo. PDGF derived from HCC cells has a capacity to activate Ras/ERK signaling pathway of TC as a result of accelerating MMP-9 expression, but it’s no significant for proliferative potential and apoptotic rate of TCs. While tyrosine kinase inhibitors and miR-942-3p suppress MMP-9 expression to make loss functions of TCs. Various mutations of TCs are also tested and single nucleotide polymorphisms of MMP-9 may be the potentially molecular mechanism of increasing protein expression in the invasive process of HCC. Conclusion: Our results demonstrate two potential mechanisms between HCC cells and TCs, suggesting that TC is a novel marker and target on deciphering reasons of cancer metastasis.

scholarly journals Multi-Omics Integrative Analysis Uncovers Molecular Subtypes and mRNAs as Therapeutic Targets for Liver Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Yi Shen ◽  
Wei Xiong ◽  
Qi Gu ◽  
Qin Zhang ◽  
Jia Yue ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Molecular Subtypes ◽  
Therapeutic Targets ◽  
Clinical Information ◽  
Copy Number Variations ◽  
The Cancer Genome Atlas ◽  
Liver Carcinoma ◽  
Normal Tissues ◽  
Omics Analysis ◽  
Cancer Tissues

Objective: This study aimed to systematically analyze molecular subtypes and therapeutic targets of liver cancer using integrated multi-omics analysis.Methods: DNA copy number variations (CNVs), simple nucleotide variations (SNVs), methylation, transcriptome as well as corresponding clinical information for liver carcinoma were retrieved from The Cancer Genome Atlas (TCGA). Multi-omics analysis was performed to identify molecular subtypes of liver cancer via integrating CNV, methylation as well as transcriptome data. Immune scores of two molecular subtypes were estimated using tumor immune estimation resource (TIMER) tool. Key mRNAs were screened and prognosis analysis was performed, which were validated using RT-qPCR. Furthermore, mutation spectra were analyzed in the different subtypes.Results: Two molecular subtypes (iC1 and iC2) were conducted for liver cancer. Compared with the iC2 subtype, the iC1 subtype had a worse prognosis and a higher immune score. Two key mRNAs (ANXA2 and CHAF1B) were significantly related to liver cancer patients' prognosis, which were both up-regulated in liver cancer tissues in comparison to normal tissues. Seventeen genes with p < 0.01 differed significantly for SNV loci between iC1 and iC2 subtypes.Conclusion: Our integrated multi-omics analyses provided new insights into the molecular subtypes of liver cancer, helping to identify novel mRNAs as therapeutic targets and uncover the mechanisms of liver cancer.

scholarly journals Downregulation of HBx Restrains Proliferation, Migration, and Invasion of HepG2 Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Chaoqun Huang ◽  
Wei Liu ◽  
Xiaochuan Zhao ◽  
Libin Zhao ◽  
Fuxiang Wang
Keyword(s):  
Liver Cancer ◽  
Cancer Progression ◽  
Hepg2 Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Mechanistic Study ◽  
Migration And Invasion ◽  
Cancer Pathogenesis ◽  
Induced Apoptosis ◽  
Cancer Tissues

Liver cancer is a major contributor to cancer-related death with poor survival for sufferers. Meanwhile, Hepatic B virus X protein (HBx) and XB130 are likely to participate in the pathogenesis of liver cancer. However, the detailed mechanism of HBx/XB130 in liver cancer remains to be further investigated. Our study explored the effects of HBx/XB130 on liver cancer progression. HBx and XB130 expression was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. Overexpression of HBx and XB130 was found in liver cancer tissues and cells. Mechanistic study revealed that HBx could bind to and positively regulate XB130 in HepG2 cells. Subsequently, HBx expression was knocked down, while XB130 was overexpressed in HepG2 cells in order to observe the specific role of HBx/XB130 in liver cancer in vitro. Results of CCK-8, Transwell, wound healing, and colony formation assays suggested that HBx could mediate biological function of HepG2 cells by activating the XB130-mediated PI3K/AKT pathway. In summary, our data illustrate that inhibition of HBx effectively suppressed proliferation and metastasis and induced apoptosis of liver cancer cells, which might be partially reversed by XB130. HBx and XB130 may be potential targets for liver cancer pathogenesis.

scholarly journals The Heterogeneity of Liver Cancer Metabolism

2021 ◽  
pp. 127-136
Author(s):  
Javier Salazar ◽  
Anne Le
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Cancer Metabolism ◽  
Primary Liver Cancer ◽  
Cancer Death ◽  
The World ◽  
Advanced Stages ◽  
New Biomarkers ◽  
Cancer Tissues

AbstractPrimary liver cancer is the fourth leading cause of cancer death around the world. Histologically, it can be divided into two major groups, hepatocellular carcinoma (75% of all liver cancer) and intrahepatic cholangiocarcinoma (15% of all liver cancer) [1, 2]. Primary liver cancer usually happens in liver disease or cirrhosis patients [1], and the risk factors for developing HCC depend on the etiology [3] and the country of provenance [1]. There is an urgent need for an accurate diagnostic test given the high proportion of false positives and false negatives for alpha-fetoprotein (AFP), a common HCC biomarker [4]. Due to often being diagnosed in advanced stages, HCCrelated deaths per year have doubled since 1999 [3]. With the use of metabolomics technologies [5], the aberrant metabolism characteristics of cancer tissues can be discovered and exploited for the new biomarkers and new therapies to treat HCC [6, 7].

scholarly journals VEGF Family Gene Expression as Prognostic Biomarkers for Alzheimer’s Disease and Primary Liver Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Kai Xu ◽  
Chuan-ling Wu ◽  
Zhi-xin Wang ◽  
Hai-jiu Wang ◽  
Feng-jiao Yin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Liver Cancer ◽  
Gene Set Enrichment Analysis ◽  
Prognostic Biomarkers ◽  
Vegf Expression ◽  
Immune Infiltration ◽  
Cancer Tissues ◽  
The Relationship

Background. To analyze the expression of vascular endothelial growth factor (VEGF) in hepatocellular carcinoma (HCC) and cognitive impairment, explore the relationship between the expression of VEGF family genes and prognosis of patients with HCC, and evaluate the predictive ability of VEGF in cognitive impairment using computerized methods. Methods. VEGF expression in liver cancer tissues and normal tissues was analyzed using bioinformatics methods. The Kaplan-Meier survival analysis method was also used to analyze the relationship between VEGF expression and the prognosis of patients with HCC. Furthermore, immune infiltration assessment and gene set enrichment analysis were performed. Meanwhile, the differential expression of VEGF family genes between patients with Alzheimer’s disease (AD) and healthy controls was also checked. Results. Based on The Cancer Genome Atlas (TCGA) database, the VEGF family genes (VEFGA, VEGFB, VEGFC, and VEGFD) were highly expressed in cancer tissues and were significantly associated with poor prognosis in HCC. In HCC, the VEGF family genes showed significant heterogeneity in their functional and immune infiltration characteristics. Finally, VEGF family genes were identified as prognostic biomarkers in AD and risk prediction markers in HCC. Conclusions. VEGF is highly expressed in patients with HCC and lowly expressed in patients with AD. VEGF has opposite opposing roles in the treatment of tumors and cognitive impairment.

Artificial intelligence-based pathology for gastrointestinal and hepatobiliary cancers

Gut ◽  
2020 ◽  
pp. gutjnl-2020-322880 ◽  
Author(s):  
Julien Calderaro ◽  
Jakob Nikolas Kather
Keyword(s):  
Artificial Intelligence ◽  
Liver Cancer ◽  
Genetic Alterations ◽  
Clinical Implications ◽  
Complex Information ◽  
Wide Range ◽  
Depth Analysis ◽  
Cancer Types ◽  
Cancer Tissues ◽  
Very High

Artificial intelligence (AI) can extract complex information from visual data. Histopathology images of gastrointestinal (GI) and liver cancer contain a very high amount of information which human observers can only partially make sense of. Complementing human observers, AI allows an in-depth analysis of digitised histological slides of GI and liver cancer and offers a wide range of clinically relevant applications. First, AI can automatically detect tumour tissue, easing the exponentially increasing workload on pathologists. In addition, and possibly exceeding pathologist’s capacities, AI can capture prognostically relevant tissue features and thus predict clinical outcome across GI and liver cancer types. Finally, AI has demonstrated its capacity to infer molecular and genetic alterations of cancer tissues from histological digital slides. These are likely only the first of many AI applications that will have important clinical implications. Thus, pathologists and clinicians alike should be aware of the principles of AI-based pathology and its ability to solve clinically relevant problems, along with its limitations and biases.

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