scholarly journals Expression and Clinical Significance of the Novel Long Noncoding RNA ZNF674-AS1 in Human Hepatocellular Carcinoma

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Lufei Zhang ◽  
Tianyu He ◽  
Yingcai Yan ◽  
Yuan Zhang ◽  
Xiaohu Zhou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Noncoding Rna ◽  
Clinical Stage ◽  
Normal Liver ◽  
Expression Level ◽  
The Novel ◽  
Normal Liver Cell ◽  
Normal Tissues ◽  
Cancer Occurrence ◽  
Kaplan Meier

Long noncoding RNAs (lncRNAs) play crucial roles in cancer occurrence and progression. However, the relationship between the expression levels of lncRNAs and the hepatocellular carcinoma (HCC) process is unclear. The goal of this study was to determine the expression level of ZNF674-AS1, a newly found lncRNA, in HCC and its clinical association. The expression of ZNF674-AS1 in 137 pairs of tumorous and adjacent normal tissues from patients with HCC was detected by quantitative real-time reverse transcription polymerase chain reaction. Additionally, the potential associations between its level in HCC tissue and clinicopathological features were analyzed. The expression of ZNF674-AS1 in the HCC cell lines HepG2, HCCLM3, SK-Hep1, HuH7, Hep3B, and MHCC97H was significantly downregulated compared with that in the normal liver cell line QSG-7701. The expression of ZNF674-AS1 was downregulated in 72% (99/137) of HCC tissues compared with that in paired adjacent normal tissues (p<0.01). The results showed that the ZNF674-AS1 expression level was significantly correlated with metastasis (p=0.041), clinical stage (p=0.039), and histopathologic grading (p=0.045). In addition, the Kaplan–Meier survival curves revealed that low ZNF674-AS1 expression was associated with poor prognosis in patients with HCC. Our data suggest that ZNF674-AS1 may play some role during cancer occurrence and progression and may be a new biomarker for HCC.

scholarly journals Low Expression of KAT6B May Affect Prognosis in Hepatocellular Carcinoma

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Junjie Jiang ◽  
Hui-Ju Wang ◽  
Xiao-Zhou Mou ◽  
Huanqing Zhang ◽  
YiZhen Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Normal Liver ◽  
Clinicopathological Parameters ◽  
Expression Array ◽  
Chi Square ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Chi Square Test ◽  
The Relationship ◽  
Liver Tissues

Aims: Lysine acetyltransferase 6B (KAT6B), is a histone acetyltransferase implicated to have a role in tumor suppression. However, the relationship between KAT6B and hepatocellular carcinoma (HCC) is unclear. The purpose of this study was to detect the expression of KAT6B in HCC tissues and analyze its connection with the clinicopathological features of HCC. Methods: First, we performed immunohistochemical staining on 250 HCC tissues and 222 non-tumor liver tissues to examine the expression of KAT6B.Then the relation between KAT6B expression and clinicopathological parameters was analyzed by chi-square test, and the overall survival analysis was conducted by Kaplan-Meier survival method. In addition, based on the Oncomine expression array online and the UALCAN database, we compared KAT6B expression differences between normal liver tissues and HCC tissues more broadly. Results: Compared with normal tissues, KAT6B expression was significantly lower in HCC tissues. Low KAT6B expression was found to be related to gender, AFP level, and tumor size. According to the online database, KAT6B expression was found to be decreased in HCC tissues and high in normal tissues. Conclusions: Lower expression of KAT6B is associated with poor prognosis of HCC, and KAT6B may be a potential tumor suppressor in liver cancer.

Decreased expression of long non-coding LOC285194 predicts tumour progression and poor prognosis of hepatocellular carcinoma after curative hepatectomy

2019 ◽  
Vol 96 (1132) ◽  
pp. 79-83 ◽  
Author(s):  
Jianguo Qiu ◽  
Gang Pan ◽  
Ming Li
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Tumour Progression ◽  
Disease Free Survival ◽  
Normal Liver ◽  
Expression Level ◽  
Term Survival ◽  
Normal Liver Cell ◽  
Low Expression

BackgroundLong non-coding RNAs (LncRNAs) have been recently implicated as having oncogenic and tumour suppressor roles. LncRNA LOC285194 (LOC285194) expression was significantly reduced in a variety of tumour tissues and cell lines, which promotes cell proliferation and migration. The aim of the present study is to examine the expression pattern of LOC285194 and its clinical significance in hepatocellular carcinoma (HCC) patients after curative liver resection.Materials and methodsWe examined the expression of LOC285194 in 120 HCC samples and controls from adjacent non-tumour tissues using real-time quantitative reverse transcription-PCR and analysed its correlation with clinical parameters and prognosis in these patients who have undergone curative hepatic resection with a median follow-up of 3.5 years.ResultsThe expression level of LOC285194 was significantly lower in tumour tissues and four liver cancer cell lines compared with adjacent normal tissues and normal liver cell line. Furthermore, a low expression of LOC285194 was significantly correlated with advanced tumour stage, microvascular invasion, tumour number and differentiation. Additionally, survival analysis showed that patients with low LOC285194 expression had a significantly worse overall and disease-free survival. Moreover, univariate and multivariate analyses showed that decreased expression of LOC285194 was an independent predictor of long-term survival.ConclusionsThe low expression level of LOC285194 might be a novel candidate biomarker for predicting tumour progression and poor prognosis in HCC patients who have undergone hepatectomy and might be a potential target for gene therapy.

scholarly journals Prognostic value of members of the HSP70 family in Hepatocellular Carcinoma

2020 ◽  
Author(s):  
Haixing Jiang ◽  
Ziyu Liang ◽  
Shanyu Qin ◽  
Kang Liu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Drug Targets ◽  
Hepatitis Virus ◽  
Clinical Stage ◽  
Normal Liver ◽  
Normal Tissues ◽  
Hsp70 Family ◽  
Ppi Networks ◽  
Close Relationship ◽  
Km Plotter

Abstract BACKGROUND: Despite multiple functions in the disease, the prognosis of the heat shock protein (HSP) 70 family in Hepatocellular Carcinoma (HCC) remains unclear. METHODS: The UALCAN database has provided information about the expression level of HSP70 family members in both HCC and in normal tissues. Overall survival (OS) was conducted by Kaplan-Meier plotter (KM plotter). Gene ontology (GO) and KEGG pathway enrichment analyses were accomplished by DAVID database. GeneMANIA and STRING were applied to construct gene-gene and protein-protein interaction (PPI) networks. RESULTS: From the UALCAN database, we found that the expression levels of eight members of the HSP70 family in HCC patients were higher than in normal liver tissues. These eight members were, namely, HSPA1A, HSPA1B, HSPA1L, HSPA2, HSPA5, HSPA6, HSPA8 and HSPA9. From KM plotter database, high expression of HSPA1A, HSPA1B, HSPA6 and HSPA8 has been observed to be associated with worse OS in patients with HCC (hazard ratio [HR] =1.49, 95% confidence interval [CI]: 1.03-2.15, P=0.031; HR=1.49, 95%CI: 1.05-2.12, P=0.026; HR=1.53, 95%CI: 1.06-2.2, P=0.021 and HR=1.81, 95%CI: 1.21-2.71, P=0.0036, respectively). We also found that the high expressions of HSPA1A, HSPA1B, HSPA6 and HSPA8 were related to unfavorable OS of HCC patients with other factors such as clinical stage, gender, race and hepatitis virus. From GO and KEEG analysis, we detected a close relationship between these eight genes and Biological process, Cellular component, Molecular function and cancer related signaling pathways. The PPI network and GeneMANIA results showed that there was a strong co-expression relationship between the protein homology and the genes. CONCLUSIONS: According to previous studies and analysis, when HSPA1A, HSPA1B, HSPA6 and HSPA8 were highly expressed in HCC patients, they generally demonstrated lower OS. Therefore, the members of HSP70 family are likely to be used as drug targets and prognostic biomarkers when treating HCC patients.

scholarly journals Selective Anti-Cancer Effects of Plasma-Activated Medium and Its High Efficacy with Cisplatin on Hepatocellular Carcinoma with Cancer Stem Cell Characteristics

2021 ◽  
Vol 22 (8) ◽  
pp. 3956
Author(s):  
Yan Li ◽  
Tianyu Tang ◽  
Hae June Lee ◽  
Kiwon Song
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Cell Lines ◽  
Primary Liver Cancer ◽  
Atmospheric Pressure Plasma ◽  
Normal Liver ◽  
Normal Liver Cell ◽  
Ample Evidence ◽  
Huh7 Cells ◽  
Anti Cancer

Hepatocellular carcinoma (HCC) is a major histological subtype of primary liver cancer. Ample evidence suggests that the pathological properties of HCC originate from hepatic cancer stem cells (CSCs), which are responsible for carcinogenesis, recurrence, and drug resistance. Cold atmospheric-pressure plasma (CAP) and plasma-activated medium (PAM) induce apoptosis in cancer cells and represent novel and powerful anti-cancer agents. This study aimed to determine the anti-cancer effect of CAP and PAM in HCC cell lines with CSC characteristics. We showed that the air-based CAP and PAM selectively induced cell death in Hep3B and Huh7 cells with CSC characteristics, but not in the normal liver cell line, MIHA. We observed both caspase-dependent and -independent cell death in the PAM-treated HCC cell lines. Moreover, we determined whether combinatorial PAM therapy with various anti-cancer agents have an additive effect on cell death in Huh7. We found that PAM highly increased the efficacy of the chemotherapeutic agent, cisplatin, while enhanced the anti-cancer effect of doxorubicin and the targeted-therapy drugs, trametinib and sorafenib to a lesser extent. These findings support the application of CAP and PAM as anti-cancer agents to induce selective cell death in cancers containing CSCs, suggesting that the combinatorial use of PAM and some specific anti-cancer agents is complemented mechanistically.

scholarly journals Cyclin-Dependent Kinase Regulatory Subunit 2 Indicated Poor Prognosis and Facilitated Aggressive Phenotype of Hepatocellular Carcinoma

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Jie Zhang ◽  
Qianqian Song ◽  
Jinxia Liu ◽  
Lina Lu ◽  
Yuqing Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Poor Prognosis ◽  
Disease Free Survival ◽  
Normal Liver ◽  
Regulatory Subunit ◽  
Mrna Levels ◽  
Cyclin Dependent Kinase ◽  
Normal Tissues ◽  
Hcc Cells

Cyclin-dependent kinase regulatory subunit 2 (CKS2) is a member of the cell cycle-dependent protein kinase subunit family, which is implicated as an oncogene in various malignancies. However, the clinical significance, oncogenic functions, and related mechanisms of CKS2 in hepatocellular carcinoma (HCC) remain largely unclear. In the present study, expression features and prognostic value of CKS2 were evaluated in the bioinformatic databases and HCC tissues. The effects of CKS2 on the malignant phenotypes of HCC cells were explored in vitro. According to the analyses of three bioinformatic databases, mRNA levels of CKS2 were elevated in HCC tissues compared with the normal tissues. Immunohistochemical assays found that high CKS2 expression was closely associated with liver cirrhosis (P=0.019), poor differentiation (P=0.02), portal vein invasion (P<0.001), TNM stage (P=0.019), tumor metastasis (P=0.008), and recurrence (P=0.003). The multivariate regression analyses suggested that CKS2 was an independent prognostic factor for overall survival (HR=2.088, P=0.014) and disease-free survival (HR=2.511, P=0.002) of HCC patients. Moreover, the bioinformatic analyses indicated that CKS2 might be associated with the malignant phenotypes in HCC progression. In addition, in vitro assays showed that CKS2 expression was higher in HCC cell lines than in normal liver cells. Knockdown of CKS2 remarkably repressed the proliferation, colony formation (P=0.0003), chemoresistance, migration (P=0.0047), and invasion (P=0.0012) of HCC cells. Taken together, overexpression of CKS2 was significantly correlated with poor prognosis of HCC patients and the malignant phenotypes of HCC cells, suggesting that it was a novel prognostic biomarker and potential target of HCC.

scholarly journals Functional lncRNA-miRNA-mRNA Networks in Response to Baicalein Treatment in Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Xin Zhao ◽  
Dongyang Tang ◽  
Xiaofei Chen ◽  
Shaoqing Chen ◽  
Cheng Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Treatment Group ◽  
Cancer Progression ◽  
Messenger Rna ◽  
Noncoding Rna ◽  
Mirna Targets ◽  
Kaplan Meier ◽  
Dmso Treatment ◽  
Human Protein Atlas ◽  
Kaplan Meier Plotter

Introduction. Baicalein has been shown to have antitumor activities in several cancer types. However, its acting mechanisms remain to be further investigated. This work is aimed at exploring the functional long noncoding RNA (lncRNA)/microRNA (miRNA)/messenger RNA (mRNA) triplets in response to baicalein in hepatocellular carcinoma (HCC) cell to understand the mechanisms of baicalein in HCC. Methods. Differentially expressed lncRNAs (DELs) and miRNAs (DEMs) in HCC cell treated with baicalein were first screened using GSE95504 and GSE85511, respectively. miRNA targets for DELs were predicted and intersected with DEMs, after which the miRNA expression was validated using ENCORI and its prognostic value was assessed using Kaplan-Meier plotter. Potential miRNA targets were predicted by 3 prediction tools, after which expression level was validated at UALCAN and Human Protein Atlas. Kaplan-Meier plotter was used to evaluate the effects of these genes on overall survival and recurrence-free survival of HCC patients. Enrichment analyses for these genes were performed at DAVID. Results. Here, we identified 14 overlapping DELs and 26 overlapping DEMs in the baicalein treatment group than those in the DMSO treatment group. Subsequently, by analyzing expression and clinical significance of miRNAs, hsa-miR-4443 was found as a highly potential miRNA target. Then, targets of hsa-miR-4443 were predicted and analyzed, and we found AKT1 was the most potential target for hsa-miR-4443. Hence, the lncRNAs-hsa-miR-4443-AKT1 axis that can respond to baicalein was established. Conclusion. Collectively, we elucidated a role of lncRNAs-hsa-miR-4443-AKT1 pathway in response to baicalein treatment in HCC, which could help us understand the roles of baicalein in inhibiting cancer progression and may provide novel insights into the mechanisms behind HCC progression.

scholarly journals Long non-coding RNA LINC00641 promotes the growth and invasiveness of hepatocellular carcinoma by antagonizing miR-501-3p

2021 ◽  
Author(s):  
Haitao Xie ◽  
Hui Zhou ◽  
Yan Jiang ◽  
Wenqian Xu ◽  
Leping Zeng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Normal Liver ◽  
In Vivo Studies ◽  
Luciferase Reporter ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion ◽  
Hcc Cells

IntroductionLong non-coding RNA LINC00641 has been reported to regulate tumor progression in several cancers. However, the expression and function of LINC00641 in hepatocellular carcinoma (HCC) is still unclear.Material and methodsIn this study, we measured the expression of LINC00641 in 79 pairs of HCC and adjacent normal liver tissues. The clinical significance of LINC00641 in HCC was explored. We also investigated the function of LINC00641 in HCC proliferation and invasion.ResultsWe observed that LINC00641 expression was significantly increased in HCC relative to normal tissues (P < 0.0001). High expression of LINC00641 was significantly associated with vascular invasion, advanced TNM stage, and reduced overall survival in HCC patients. Knockdown of LINC00641 inhibited the proliferation, colony formation, and invasion of HCC cells. In contrast, overexpression of LINC00641 promoted HCC cell growth and invasiveness. In vivo studies confirmed that knockdown of LINC00641 restrained tumorigenesis of HCC cells. Mechanistic studies revealed that LINC00641 inhibited the expression of miR-501-3p, which has been previously reported to act as a tumor suppressor in HCC. Furthermore, luciferase reporter assays validated that LINC00641 harbored a target site for miR-501-3p. Rescue experiments demonstrated that LINC00641-induced proliferation and invasion of HCC cells was reversed by co-expression of miR-501-3p.ConclusionsTaken together, LINC00641 contributes to aggressive phenotype of HCC cells by sponging miR-501-3p and represents a promising therapeutic target for this disease.

scholarly journals The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer

2017 ◽  
Vol 41 (2) ◽  
pp. 635-644 ◽  
Author(s):  
Jian Xu ◽  
Rui Zhang ◽  
Jian Zhao
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Proliferation Rate ◽  
Expression Level ◽  
The Novel ◽  
Cell Proliferation Rate ◽  
Potential Tumor Suppressor

Background/Aims: The novel long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) has been reported as a potential tumor suppressor, while the functional role of TUSC7 is still unknown in colorectal cancer (CRC). Here, we characterized TUSC7 expression profile in CRC patients and investigated its biological function and potential molecular mechanism. Methods: RNA isolation, qRT-PCR, cell counter kit-8 assay, cell cycle assay, EdU assay, and western blot were performed. Statistical analyses were performed using SPSS 18.0 software and p value < 0.05 was considered as statistically significant. Results: In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). Patients with high expression of TUSC7 had better survival than those with low expression of TUSC7 (HR = 0.342, 95% CI: 0.120-0.972, P = 0.044). Cell count kit 8 and EdU assays showed that ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. After silence of TUSC7 with small interfering RNA, cell proliferation rate increased. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. Conclusion: To summary, we demonstrated that TUSC7 is a potential tumor suppressor in CRC, and TUSC7 could inhibit CRC cell proliferation by completely sponging miR-211-3p.

scholarly journals Identification of the Novel Oncogenic Role of SAAL1 and Its Therapeutic Potential in Hepatocellular Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1843
Author(s):  
Pei-Yi Chu ◽  
Shiao-Lin Tung ◽  
Kuo-Wang Tsai ◽  
Fang-Ping Shen ◽  
Shih-Hsuan Chan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Therapeutic Potential ◽  
The Cancer Genome Atlas ◽  
The Novel ◽  
Advanced Hcc ◽  
Independent Prognostic Marker ◽  
Normal Tissues ◽  
Amyloid A ◽  
Mtor Phosphorylation ◽  
And Migration

Hepatocellular carcinoma (HCC) is the third leading cause of cancer deaths worldwide, affecting over 700,000 people per year. The treatment effect in advanced HCC is still disappointing and prognosis of advanced HCC remains poor. Hence, to find more effective therapeutic targets to improve the treatment outcome of HCC is of urgent need. In this study, we reported the novel oncogenic function of SAAL1 (serum amyloid A-like 1) in HCC, which previously is considered as an inflammation-related gene. We found that SAAL1 was significantly upregulated in HCC tumor tissues when compared to the adjacent normal tissues and high expression of SAAL1 correlated with shorter overall survival in The Cancer Genome Atlas (TCGA) HCC database. Functionally, we showed that the depletion of SAAL1 significantly reduced cell proliferation, 3D colony formation, and migration/invasion abilities of HCC cancer cells. Furthermore, suppression of SAAL1 impaired the HGF/Met-driven Akt/mTOR phosphorylation cascade and increased the chemosensitivity of HCC cells to sorafenib and foretinib treatment. Our data indicated that SAAL1 plays an important role in HCC via mediating oncogenic HGF/Met-driven Akt/mTOR signaling and could serve as an independent prognostic marker, as well as a promising therapeutic target for HCC patients.

scholarly journals TXNRD1 Is an Unfavorable Prognostic Factor for Patients with Hepatocellular Carcinoma

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Binsheng Fu ◽  
Wei Meng ◽  
Xiancheng Zeng ◽  
Hui Zhao ◽  
Wei Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prognostic Factor ◽  
Clinical Stage ◽  
Thioredoxin Reductase ◽  
Immunohistochemical Analysis ◽  
Independent Prognostic Factor ◽  
Clinical Samples ◽  
Kaplan Meier ◽  
Thioredoxin Reductase 1 ◽  
N Classification

Thioredoxin reductase 1 (TXNRD1) which is a selenocysteine-containing protein is overexpressed in many malignancies. Its role in the hepatocellular carcinoma (HCC) prognosis has not been investigated. In this study, we investigated whether TXNRD1 functions as an independent prognostic factor for HCC patients. We found TXNRD1 was overexpressed in HCC tissues and cells, immunohistochemical analysis suggested TXNRD1 was elevated in 57 of 120 (47.5%) clinical samples, and its level was increased with the increasing clinical stage. In addition, TXNRD1 expression was positively correlated with clinical stage (p=3.5e-5), N classification (p=4.4e-4), and M classification (p=0.037) of HCC patients. Kaplan-Meier analysis revealed that patients with high TXNRD1 expression had significantly shorter survival time than patients with low TXNRD1 expression. Multivariate analysis found TXNRD1 was an independent prognostic factor for HCC patients. In conclusion, our data suggested that TXNRD1 was a biomarker for the prognosis of patients with HCC.

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