scholarly journals Upregulation Mitochondrial Carrier 1 (MTCH1) Is Associated with Cell Proliferation, Invasion, and Migration of Liver Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Guolin Chen ◽  
Shanshan Mo ◽  
Di Yuan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Rna Splicing ◽  
Enrichment Analysis ◽  
Tumor Stage ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mitochondrial Carrier ◽  
Invasion And Migration ◽  
Liver Hepatocellular Carcinoma

Among the primary causes of cancer-associated death in the world, liver hepatocellular carcinoma (LIHC) ranks the third. LIHC is defined as the sixth most frequently diagnosed carcinoma. The gene mitochondrial carrier 1 (MTCH1) is a protein-coding gene. Recent research suggests that MTCH1 may be associated with some diseases. Here, our study attempts to explore the role and implication of MTCH1 in LIHC. Kaplan Meier Plotter and GEPIA (Gene Expression Profiling Interactive Analysis) databases were employed to determine the expression of MTCH1 and its correlation with prognostic status in LIHC patients. For the first time, our results suggested that MTCH1 was aberrantly expressed in human pan-cancer and highly expressed in LIHC. Its high expression was closely associated with metastasis of tumor, stage of cancer, and poor survival of patients. Then, through enrichment analysis, MTCH1 was found to be closely related to RNA splicing in LIHC. Subsequently, we conducted a series of functional experiments. PCR data showed that LIHC cell lines and samples are highly expressed MTCH1. CCK-8 (Cell Counting Kit-8) assays and Transwell assays indicated that silencing MTCH1 certainly suppressed cell proliferation, migration, and invasion. These findings shed the clue that MTCH1 could be regarded as the potential prognosis biomarker of LIHC and a promising therapeutic target for LIHC.

scholarly journals MiR-3150b inhibits hepatocellular carcinoma cell proliferation, migration and invasion by targeting GOLPH3

2019 ◽  
Vol 68 (3) ◽  
pp. 770-775
Author(s):  
Yi Zhang ◽  
Jianjun Wang ◽  
Hongling Su
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Carcinoma Cell ◽  
Cell Counting ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Hepatocellular Carcinoma Cell ◽  
And Migration ◽  
Hcc Cells

BackgroundIn this study, we aimed to explore the potential involvement of miR-3150b in hepatocellular carcinoma (HCC) carcinogenesis.MethodsThe expression of miR-3150b and Golgi phosphoprotein 3 (GOLPH3) was determined in HCC cell lines. Cell proliferation, migration and invasion were estimated by Cell Counting Kit-8, wound healing and Transwell assays. The association between miR-3150b and GOLPH3 was verified by luciferase assay.ResultsMiR-3150b was downregulated, while GOLPH3 was remarkably upregulated in HCC cells. Furthermore, miR-3150b inhibited HCC cell proliferation, migration and invasion. MiR-3150b directly targeted and negatively regulated GOLPH3.ConclusionMiR-3150b suppressed HCC cell proliferation, invasion and migration by targeting GOLPH3.

miR-369-3p serves as prognostic factor and regulates cancer progression of hepatocellular carcinoma

2021 ◽  
Author(s):  
Can Chen ◽  
Yi Zong ◽  
Jiaojiao Tang ◽  
Ruisheng Ke ◽  
Lizhi Lv ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Pcr Analysis ◽  
Reverse Transcription Pcr ◽  
Huh7 Cells

Background: The aim of this study was to investigate the role of miR-369-3p in hepatocellular carcinoma (HCC). Materials & methods: The expression levels of miR-369-3p were detected using the quantitative real-time reverse transcription-PCR analysis. The cell counting kit-8 and transwell assays were used to explore the effects of miR-369-3p on cell proliferation, migration and invasion of HCC cells. Results: The miR-369-3p expression was downregulated in HCC tissues and cell lines, in comparison to the normal controls, respectively. In vitro, overexpression of miR-369-3p in Hep 3B and Huh7 cells inhibited cell proliferation, migration and invasion. SOX4 was a direct target of miR-369-3p. Conclusion: Our results suggested that miR-369-3p may be a tumor suppressor in HCC by targeting SOX4.

scholarly journals Identification and Validation of the N6-Methyladenosine RNA Methylation Regulator YTHDF1 as a Novel Prognostic Marker and Potential Target for Hepatocellular Carcinoma

2020 ◽  
Vol 7 ◽  
Author(s):  
Saiyan Bian ◽  
Wenkai Ni ◽  
Mengqi Zhu ◽  
Qianqian Song ◽  
Jianping Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Biological Activities ◽  
Enrichment Analysis ◽  
Cancer Genome ◽  
Gene Set Enrichment Analysis ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Rna Methylation ◽  
Hcc Cells

Purpose: N6-methyladenosine (m6A) RNA methylation has been implicated in various malignancies. This study aimed to identify the m6A methylation regulator-based prognostic signature for hepatocellular carcinoma (HCC) as well as provide candidate targets for HCC treatment.Methods: The least absolute shrinkage and selection operator (LASSO) analyses were performed to identify a risk signature in The Cancer Genome Atlas (TCGA) datasets. The risk signature was further validated in International Cancer Genome Consortium (ICGC) and Pan-Cancer Analysis of Whole Genomes (PCAWG) datasets. Following transfection of short hairpin RNA (shRNA) targeting YTHDF1, the biological activities of HCC cells were evaluated by Cell Counting Kit-8 (CCK-8), wound-healing, Transwell, flow cytometry, and xenograft tumor assays, respectively. The potential mechanisms mediated by YTHDF1 were predicted by overrepresentation enrichment analysis (ORA)/gene set enrichment analysis (GSEA) and validated by Western blotting.Results: Overexpression of m6A RNA methylation regulators was correlated with malignant clinicopathological characteristics of HCC patients. The Cox regression and LASSO analyses identified a risk signature with five m6A methylation regulators (KIAA1429, ZC3H13, YTHDF1, YTHDF2, and METTL3). In accordance with HCC cases in TCGA, the prognostic value of risk signature was also determined in ICGC and PCAWG datasets. Following analyzing the expression and clinical implications in TCGA and Gene Expression Omnibus (GEO), YTHDF1 was chosen for further experimental validation. Knockdown of YTHDF1 significantly inhibited the proliferation, migration, and invasion of HCC cells, as well as enhanced the apoptosis in vitro. Moreover, silencing YTHDF1 repressed the growth of xenograft tumors in vivo. Mechanism investigation indicated that YTHDF1 might promote the aggressive phenotypes by facilitating epithelial–mesenchymal transition (EMT) and activating AKT/glycogen synthase kinase (GSK)-3β/β-catenin signaling.Conclusion: The current study identified a robust risk signature consisting of m6A RNA methylation regulators for HCC prognosis. In addition, YTHDF1 was a potential molecular target for HCC treatment.

scholarly journals Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma

2018 ◽  
Vol 19 (7) ◽  
pp. 2029 ◽  
Author(s):  
Xiaoqi Zhang ◽  
Hao Feng ◽  
Ziyu Li ◽  
Jie Guo ◽  
Minqi Li
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Focal Adhesion ◽  
Squamous Cell ◽  
Enrichment Analysis ◽  
Migration And Invasion ◽  
Invasion And Migration

Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide. In China, its 5-year survival rate is roughly 50%, owing to acquired chemotherapeutic resistance and metastasis of the disease. Accumulating evidence demonstrates that aspirin (ASA) acts as a preventive or therapeutic agent in multiple cancers; however, anti-tumor activities induced by aspirin are unclear in OSCC. To investigate the possible role of aspirin in OSCC development, we first employed bioinformatics to analyze the anti-OSCC effects of aspirin. We performed a genetic oncology (GO) enrichment analysis using the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and the protein–protein interaction (PPI) network analysis by Cytoscape for differentially expressed genes (DEGs). We also evaluated the potential effects of aspirin on cell proliferation, invasion, migration, and apoptosis in two well-characterized OSCC cell lines (TCA8113 and CAL27). The bioinformatic results revealed that aspirin could inhibit proliferation by blocking the cell cycle, and could reduce migration and invasion via the PI3K-Akt and focal adhesion pathways. We found that ASA could downregulate the OSCC cell proliferation colony formation, invasion, and migration, as well as upregulate apoptosis. Furthermore, we found that ASA suppressed the activation of the focal adhesion kinase (FAK) and the phosphorylation of Akt, NF-κB, and STAT3. Overall, our data suggested that ASA may be developed as a chemopreventive agent to effectively treat OSCC.

MiR-3144 Suppresses Cell Proliferation, Migration, Invasion and Promotes Cell Apoptosis by Targeting Steap4 in Hepatocellular Carcinoma

2019 ◽  
Vol 9 (8) ◽  
pp. 1100-1107
Author(s):  
Qiuyuan Shi ◽  
Dandan Shen ◽  
Yuanjiang Shang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cell Apoptosis ◽  
Apoptotic Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Novel Target ◽  
Hcc Cells

Background: MicroRNAs (miRNAs) play important roles in the carcinogenesis and progression of hepatocellular carcinoma (HCC). Previous studies have shown that miR-3144 is down-regulated in HCC tissues. The present study investigated the expression and biological roles, underlying mechanisms of miR-3144 in HCC cell lines. Methods and material: RT-qPCR analysis was performed to detect miR-3144 expression in the HCC cell lines and normal hepatic cell line. CCK-8 assay showed that the effect of miR-3144 expression on cell proliferation. Using wound healing assay and Transwell assay to detect the effect of miR-3144 on cell invasion and migration of HCC. Flow cytometry assay showed that miR-3144 induced apoptotic cell death in the SK-HEP-1 cells. Luciferase reporter assay was performed to evaluate the interaction between miR-3144 and the Steap4 3′-UTR. Western blotting assay were performed to investigate the effect of miR-3144 expression on the expression of CDK2, cyclinE1, p21, MMP2, MMP9 and Steap4. Results: MiR-3144 expression was downregulated in HCC cell lines. MiR-3144 overexpression inhibited the proliferation of HCC cells via regulating CDK2, cyclinE1 and p21 in SK-HEP-1 cells. MiR-3144 suppressed the migration and invasion of HCC cells via decreasing the MMP2 and MMP9. Further, miR-3144 promotes cell apoptosis of HCC. Moreover, miR-3144 negatively regulated Steap4 expression by directly binding to the 3′-UTR of Steap4 mRNA. Conclusion: Our results suggested that miR-3144 may be a novel target for future HCC therapy.

scholarly journals SLC41A3 Exhibits as a Carcinoma Biomarker and Promoter in Liver Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Qimeng Chang ◽  
Yayun Xu ◽  
Jianfa Wang ◽  
Hui Jing ◽  
Longhua Rao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Second Primary ◽  
Solute Carrier Family ◽  
Regulatory Pathways ◽  
Solute Carrier ◽  
Liver Hepatocellular Carcinoma

Liver Hepatocellular Carcinoma (LIHC) is the fifth widely occurred carcinoma, which is thought to be the second primary contributor of carcinoma-associated death. There are almost 788,000 death tolls worldwide. Solute carrier family 41 member 3 (SLC41A3) is a member of solute carrier family 41, and it is the key point of numerous researches. Our research attempted to explore the links between SLC41A3 and LIHC through public databases. Higher expression of SLC41A3 displayed an intimate association with higher pathological stages and poorer prognosis. GO and KEGG analysis revealed the possible regulatory pathways of SLC41A3. Additionally, we carried out cell functional experiments to determine the expression of SLC41A3 in the cell lines of LIHC, as well as the effects of its silence on cell proliferation, migration, and invasion. Our data showed that SLC41A3 was greatly increased in the cell lines of LIHC. Moreover, silencing SLC41A3 impeded LIHC cell proliferation, migration, and invasion in vitro. Collectively, our study demonstrated that highly expressed SLC41A3 was a probable indication of LIHC occurrence, and SLC41A3 could be regarded as a prospective target in the treatment of LIHC.

scholarly journals Network Pharmacology and Pharmacological Evaluation Reveals the Mechanism of the Sanguisorba Officinalis in Suppressing Hepatocellular Carcinoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Nan Jiang ◽  
Hong Li ◽  
Yueshan Sun ◽  
Jing Zeng ◽  
Fei Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Signaling Pathways ◽  
Enrichment Analysis ◽  
Mapk Signaling ◽  
Migration And Invasion ◽  
Network Pharmacology ◽  
Therapeutic Effects ◽  
Sanguisorba Officinalis

Background:Sanguisorba Officinalis L. (SO) is a well-known traditional Chinese medicine (TCM), commonly applied to treat complex diseases, such as anticancer, antibacterial, antiviral, anti-inflammatory, anti-oxidant and hemostatic effects. Especially, it has been reported to exert anti-tumor effect in various human cancers. However, its effect and pharmacological mechanism on hepatocellular carcinoma (HCC) remains unclear.Methods: In this study, network pharmacology approach was applied to characterize the underlying mechanism of SO on HCC. Active compounds and potential targets of SO, as well as related genes of HCC were obtained from the public databases, the potential targets and signaling pathways were determined by protein-protein interaction (PPI), gene ontology (GO) and pathway enrichment analyses. And the compound-target and target-pathway networks were constructed. Subsequently, in vitro experiments were also performed to further verify the anticancer effects of SO on HCC.Results: By using the comprehensive network pharmacology analysis, 41 ingredients in SO were collected from the corresponding databases, 12 active ingredients screened according to their oral bioavailability and drug-likeness index, and 258 potential targets related to HCC were predicted. Through enrichment analysis, SO was found to show its excellent therapeutic effects on HCC through several pathways, mainly related to proliferation and survival via the EGFR, PI3K/AKT, NFκB and MAPK signaling pathways. Additionally, in vitro, SO was found to inhibit cell proliferation, induce apoptosis and down-regulate cell migration and invasion in various HCC cells. Moreover, western blot analysis showed that SO treatment down-regulated the expression of p-EGFR, p-PI3K, p-AKT, p-NFκB and p-MAPK proteins in HepG2 cells. These results validated that SO exerted its therapeutic effects on HCC mainly by the regulation of cell proliferation and survival via the EGFR/MAPK and EGFR/PI3K/AKT/NFκB signaling pathways.Conclusion: Taken together, this study, revealed the anti-HCC effects of SO and its potential underlying therapeutic mechanisms in a multi-target and multi-pathway manner.

scholarly journals Study of the G Protein Nucleolar 2 Value in Liver Hepatocellular Carcinoma Treatment and Prognosis

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yiwei Dong ◽  
Qianqian Cai ◽  
Lisheng Fu ◽  
Haojie Liu ◽  
Mingzhe Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
G Protein ◽  
Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Functional Assays ◽  
Close Relationship ◽  
Cancer Genome Atlas ◽  
And Function ◽  
Liver Hepatocellular Carcinoma

LIHC (liver hepatocellular carcinoma) mostly occurs in patients with chronic liver disease. It is primarily induced by a vicious cycle of liver injury, inflammation, and regeneration that usually last for decades. The G protein nucleolar 2 (GNL2), as a protein-encoding gene, is also known as NGP1, Nog2, Nug2, Ngp-1, and HUMAUANTIG. Few reports are shown towards the specific biological function of GNL2. Meanwhile, it is still unclear whether it is related to the pathogenesis of carcinoma up to date. Here, our study attempts to validate the role and function of GNL2 in LIHC via multiple databases and functional assays. After analysis of gene expression profile from The Cancer Genome Atlas (TCGA) database, GNL2 was largely heightened in LIHC, and its overexpression displayed a close relationship with different stages and poor prognosis of carcinoma. After enrichment analysis, the data revealed that the genes coexpressed with GNL2 probably participated in ribosome biosynthesis which was essential for unrestricted growth of carcinoma. Cell functional assays presented that GNL2 knockdown by siRNA in LIHC cells MHCC97-H and SMCC-7721 greatly reduced cell proliferation, migration, and invasion ability. All in all, these findings capitulated that GNL2 could be a promising treatment target and prognosis biomarker for LIHC.

scholarly journals Upregulation of miR-1266-5p serves as a prognostic biomarker of hepatocellular carcinoma and facilitates tumor cell proliferation, migration and invasion

2021 ◽  
Author(s):  
Yan Su ◽  
Ruizhu Xie ◽  
Qinyan Xu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Poor Prognosis ◽  
Prognostic Value ◽  
Tnm Stage ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Elevated Expression ◽  
Hcc Cells

Objective: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. This study aimed to analyze the prognostic value of microRNA-1266-5p (miR-1266-5p) in HCC patients and investigate its biological function in HCC progression. Methods: The expression of miR-1266-5p in tissues and cells was measured by quantitative real-time PCR (qRT-PCR). Cell counting kit-8 (CCK-8) assay was used to detect HCC cell proliferation. Transwell assay was performed to evaluate the migration and invasion of HCC cells. Kaplan-Meier methods and Cox regression analysis were used to assess the prognostic value of miR-1266-5p in HCC patients. The relationship between miR-1266-5p and DAB2IP was evaluated by luciferase reporter assay. Results: Relative expression of miR-1266-5p in tumor tissues, tissues from patients with advanced TNM stage (III–IV) and HCC cells was increased compared with that in corresponding control group. MiR-1266-5p expression was significantly associated with tumor size and TNM stage in HCC patients. Elevated expression of miR-1266-5p was associated with poor prognosis of HCC patients and served as an independent prognostic factor for HCC patients. Overexpression of miR-1266-5p significantly promoted, while miR-1266-5p knockdown significantly inhibited the proliferation, migration and invasion of HCC cells. DAB2IP could directly bind to the miR-1266-5p. Conclusion: Our findings indicated that elevated expression of miR-1266-5p can predict the poor prognosis of HCC patients, and promotes the proliferation, migration and invasion of HCC cells. Therefore, we predict that miR-1266-5p may be a novel biomarker and therapeutic target for the treatment of HCC.

scholarly journals B4GALT5 High Expression Associated With Poor Prognosis of Hepatocellular Carcinoma

2021 ◽  
Author(s):  
Yang Han ◽  
Zhe Li ◽  
Qi Wu ◽  
Hui Liu ◽  
Zhiqiang Sun ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Normal Tissue ◽  
Enrichment Analysis ◽  
Migration And Invasion ◽  
Clinical Samples ◽  
Poor Overall Survival ◽  
Clinical Prognosis ◽  
Immune Infiltration

Abstract Background: B4GALT5 is postulated to be an important protein in sugar metabolism that catalyzes the synthesis of lactosylceramide (LacCer). However, its role in hepatocellular carcinoma (HCC) remains unknown.Method: We characterized the expression of B4GALT5 in HCC tissue compared to normal tissue, and explored its function of B4GALT5 in HCC by enrichment analysis based on its co-expressed gene set. Next, we checked whether B4GALT5 expression is correlated to immune infiltration level and clinical prognosis in hepatocellular carcinoma. Finally, we verified the expression of B4GALT5 using clinical samples evaluated by RT-PCR, and conducted in vitro experiments with B4GALT5-knockdown HCC cells to investigate the function of B4GALT5 in the HCC cell proliferation, migration and invasion.Results: We found B4GALT5 mRNA and protein expression levels were significantly high in HCC tissue compared to normal tissue. The enrichment analysis of the gene sets that co-expressed with B4GALT5 showed specificity in HCC-related pathways and functions. Also, the expression pattern of B4GALT5 was significantly related to the immune infiltration level, especially CD4+ T cell and macrophage cells. B4GALT5 higher mRNA expression was associated with poor overall survival (OS) in HCC patients. Furthermore, In vitro experiments showed that depletion of B4GALT5 significantly inhibited HCC cell proliferation, migration and invasion. This study revealed the function and its mediated pathways of B4GALT5 in HCC, indicating that B4GALT5 may serve as a prognostic biomarker of HCC.

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