scholarly journals High PPT1 expression predicts poor clinical outcome and PPT1 inhibitor DC661 enhances sorafenib sensitivity in hepatocellular carcinoma

2021 ◽  
Author(s):  
Jianjun Xu ◽  
Zhe Su ◽  
Xiang Cheng ◽  
Shaobo Hu ◽  
Wenjie Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
T Cell Activation ◽  
Critical Role ◽  
Treatment Result ◽  
Tunel Staining ◽  
Sorafenib Treatment ◽  
Adaptive Resistance ◽  
Hcc Cells

Abstract Background Adaptive resistance and side effects of sorafenib treatment result in unsatisfied survival of patients with hepatocellular carcinoma (HCC). Palmitoyl-protein thioesterase 1 (PPT1) plays a critical role in progression of various cancers. However, its role on prognosis and immune infiltrates in HCC remains unclarified. Methods By data mining in the Cancer Genome Atlas databases, the role of PPT1 in HCC were initially investigated. Furthermore, HCC cell lines Hep 3B and Hep 1–6 were treated with DC661 against PPT1. The biological function of PPT1 was determined by CCK-8 test, colony formation assay, TUNEL staining, immunofluorescence staining, Western blotting, and PI-Annexin V apoptosis assays in vitro. Animal models of subcutaneous injection were applied to investigate the therapeutic role of targeting PPT1. Results Wefound that PPT1 levels were significantly upregulated in HCC tissues compared with normal tissues and were significantly associated with a poor prognosis. Multivariate analysis further confirmed that high expression of PPT1 was an independent risk factor for poor overall survival of HCC patients. We initially found that PPT1 was significantly upregulated in sorafenib-resistant cell lines established in this study. Upon sorafenib treatment, HCC cells acquired adaptive resistance by inducing autophagy. We found that DC661, a selective and potent small-molecule PPT1-inhibitor, induced lysosomal membrane permeability, caused lysosomal deacidification, inhibited autophagy and enhanced sorafenib sensitivity in HCC cells. Interestingly, this sensitization effect was also mediated by the induction mitochondrial pathway apoptosis. In addition, the expression level of PPT1 was associated with the immune infiltration in the HCC tumor microenvironment, and PPT1 inhibitor DC661 significantly enhanced the anti-tumor immune response by promoting dendritic cell maturation and further promoting CD8+ T cell activation. Moreover, DC661 combined with sorafenib was also very effective at treating xenograft models in immunized mice. Conclusions Our findings suggested that targeting PPT1 with DC661 in combination with sorafenib might be a novel and effective alternative therapeutic strategy for HCC.

CDK12 inhibition mediates DNA damage and is synergistic with sorafenib treatment in hepatocellular carcinoma

Gut ◽  
2019 ◽  
Vol 69 (4) ◽  
pp. 727-736 ◽  
Author(s):  
Cun Wang ◽  
Hui Wang ◽  
Cor Lieftink ◽  
Aimee du Chatinier ◽  
Dongmei Gao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Damage ◽  
Cell Lines ◽  
Synergistic Effects ◽  
Loss Of Function ◽  
Bioinformatics Analyses ◽  
Sorafenib Treatment ◽  
Hcc Cells

ObjectivesHepatocellular carcinoma (HCC) is one of the most frequent malignancies and a major leading cause of cancer-related deaths worldwide. Several therapeutic options like sorafenib and regorafenib provide only modest survival benefit to patients with HCC. This study aims to identify novel druggable candidate genes for patients with HCC.DesignA non-biased CRISPR (clustered regularly interspaced short palindromic repeats) loss-of-function genetic screen targeting all known human kinases was performed to identify vulnerabilities of HCC cells. Whole-transcriptome sequencing (RNA-Seq) and bioinformatics analyses were performed to explore the mechanisms of the action of a cyclin-dependent kinase 12 (CDK12) inhibitor in HCC cells. Multiple in vitro and in vivo assays were used to study the synergistic effects of the combination of CDK12 inhibition and sorafenib.ResultsWe identify CDK12 as critically required for most HCC cell lines. Suppression of CDK12 using short hairpin RNAs (shRNAs) or its inhibition by the covalent small molecule inhibitor THZ531 leads to robust proliferation inhibition. THZ531 preferentially suppresses the expression of DNA repair-related genes and induces strong DNA damage response in HCC cell lines. The combination of THZ531 and sorafenib shows striking synergy by inducing apoptosis or senescence in HCC cells. The synergy between THZ531 and sorafenib may derive from the notion that THZ531 impairs the adaptive responses of HCC cells induced by sorafenib treatment.ConclusionOur data highlight the potential of CDK12 as a drug target for patients with HCC. The striking synergy of THZ531 and sorafenib suggests a potential combination therapy for this difficult to treat cancer.

scholarly journals Downregulation of CRABP2 Inhibit the Tumorigenesis of Hepatocellular Carcinoma In Vivo and In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Qingmin Chen ◽  
Ludong Tan ◽  
Zhe Jin ◽  
Yahui Liu ◽  
Ze Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Retinoic Acid ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Tumor Stage ◽  
Migration And Invasion ◽  
Hcc Cells

Cellular retinoic acid-binding protein 2 (CRABP2) binds retinoic acid (RA) in the cytoplasm and transports it into the nucleus, allowing for the regulation of specific downstream signal pathway. Abnormal expression of CRABP2 has been detected in the development of several tumors. However, the role of CRABP2 in hepatocellular carcinoma (HCC) has never been revealed. The current study aimed to investigate the role of CRABP2 in HCC and illuminate the potential molecular mechanisms. The expression of CRABP2 in HCC tissues and cell lines was detected by western blotting and immunohistochemistry assays. Our results demonstrated that the expression levels of CRABP2 in HCC tissues were elevated with the tumor stage development, and it was also elevated in HCC cell lines. To evaluate the function of CRABP2, shRNA-knockdown strategy was used in HCC cells. Cell proliferation, metastasis, and apoptosis were analyzed by CCK-8, EdU staining, transwell, and flow cytometry assays, respectively. Based on our results, knockdown of CRABP2 by shRNA resulted in the inhibition of tumor proliferation, migration, and invasion in vitro, followed by increased tumor apoptosis-related protein expression and decreased ERK/VEGF pathway-related proteins expression. CRABP2 silencing in HCC cells also resulted in the failure to develop tumors in vivo. These results provide important insights into the role of CRABP2 in the development and development of HCC. Based on our findings, CRABP2 may be used as a novel diagnostic biomarker, and regulation of CRABP2 in HCC may provide a potential molecular target for the therapy of HCC.

scholarly journals Melatonin enhances the anti-tumor effect of sorafenib via AKT/p27-mediated cell cycle arrest in hepatocarcinoma cell lines

RSC Advances ◽  
2017 ◽  
Vol 7 (34) ◽  
pp. 21342-21351 ◽  
Author(s):  
Fei Long ◽  
Chengyong Dong ◽  
Keqiu Jiang ◽  
Yakun Xu ◽  
Xinming Chi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cycle Arrest ◽  
Hepatocarcinoma Cell ◽  
Proposed Model ◽  
Hcc Cells

Proposed model elucidating the role of MT in regulating the proliferation of hepatocellular carcinoma (HCC) cells treated with sorafenib.

scholarly journals Modulation of SIRT3 expression through CDK4/6 enhances the anti-cancer effect of sorafenib in hepatocellular carcinoma cells

2020 ◽  
Author(s):  
HanHee Jo ◽  
Yusun Park ◽  
Taehun Kim ◽  
Jisu Kim ◽  
JongSook Lee ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Combined Treatment ◽  
Xenograft Model ◽  
Cancer Tissue ◽  
Sorafenib Treatment ◽  
Tumor Types ◽  
Related Proteins ◽  
Sirt3 Expression ◽  
Hcc Cells

Abstract Background : Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide. The only drug currently approved for clinical use in the treatment of advanced HCC is sorafenib. However, many patients with HCC show reduced sensitivity to sorafenib during treatment. SIRT3, a member of the mammalian sirtuin family, is a tumor suppressor in certain tumor types. However, only few studies have investigated the effects of SIRT3 on tumor prognosis and sorafenib sensitivity in patients with HCC. Here, we aimed to investigate the correlation between SIRT3 expression and glucose metabolism and proliferation in HCC and discover effective compounds that increase endogenous SIRT3 modulation effect of sorafenib. Methods: To determine the correlation between SIRT3 and glucose related proteins, immunostaining was performed with liver cancer tissue using various antibodies. To investigate whether the expression of SIRT3 in HCC is related to the resistance to sorafenib, we treated sorafenib after the modulation of SIRT3 levels in HCC cell lines (overexpression in Huh7, knockdown in HepG2). We also employed PD0332991 to modulate the SIRT3 expression in HCC cell and conducted functional assays. Results: SIRT3 expression was downregulated in high glycolytic and proliferative HCC cells of human patients, xenograft model and HCC cell lines. Moreover, SIRT3 expression was downregulated after sorafenib treatment, resulting in reduced drug sensitivity in HCC cell lines. To enhance the anti-tumor effect of sorafenib, we employed PD0332991 (CDK4/6-Rb inhibitor) based on the correlation between SIRT3 and phosphorylated retinoblastoma protein in HCC. Notably, combined treatment with sorafenib and PD0332991 showed an enhancement of the anti-tumor effect in HCC cells. Conclusions: Our data suggest that the modulation of SIRT3 by CDK4/6 inhibition might be useful for HCC therapy together with sorafenib, which, unfortunately, has limited efficacy and whose use is often associated with drug resistance.

miR-541 potentiates the response of human hepatocellular carcinoma to sorafenib treatment by inhibiting autophagy

Gut ◽  
2019 ◽  
Vol 69 (7) ◽  
pp. 1309-1321 ◽  
Author(s):  
Wen-Ping Xu ◽  
Jin-Pei Liu ◽  
Ji-Feng Feng ◽  
Chang-Peng Zhu ◽  
Yuan Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Loss Of Function ◽  
Sorafenib Treatment ◽  
Transmission Electron ◽  
Reporter Assays ◽  
Hcc Cells

ObjectiveAutophagy participates in the progression of hepatocellular carcinoma (HCC) and the resistance of HCC cells to sorafenib. We investigated the feasibility of sensitising HCC cells to sorafenib by modulating miR-541-initiated microRNA-autophagy axis.DesignGain- and loss-of-function assays were performed to evaluate the effects of miR-541 on the malignant properties and autophagy of human HCC cells. Autophagy was quantified by western blotting of LC3, transmission electron microscopy analyses and confocal microscopy scanning of mRFP-GFP-LC3 reporter construct. Luciferase reporter assays were conducted to confirm the targets of miR-541. HCC xenograft tumours were established to analyse the role of miR-541 in sorafenib-induced lethality.ResultsThe expression of miR-541 was downregulated in human HCC tissues and was associated with malignant clinicopathologic phenotypes, recurrence and survival of patients with HCC. miR-541 inhibited the growth, metastasis and autophagy of HCC cells both in vitro and in vivo. Prediction software and luciferase reporter assays identified autophagy-related gene 2A (ATG2A) and Ras-related protein Rab-1B (RAB1B) as the direct targets of miR-541. Consistent with the effects of the miR-541 mimic, inhibition of ATG2A or RAB1B suppressed the malignant phenotypes and autophagy of HCC cells. Furthermore, siATG2A and siRAB1B partially reversed the enhancement of the malignant properties and autophagy in HCC cells mediated by the miR-541 inhibitor. More interestingly, higher miR-541 expression predicted a better response to sorafenib treatment, and the combination of miR-541 and sorafenib further suppressed the growth of HCC cells in vivo compared with the single treatment.ConclusionsDysregulation of miR-541-ATG2A/RAB1B axis plays a critical role in patients’ responses to sorafenib treatment. Manipulation of this axis might benefit survival of patients with HCC, especially in the context of the highly pursued strategies to eliminate drug resistance.

scholarly journals Dioscorea Zingiberensis New Saponin Inhibits the Growth of Hepatocellular Carcinoma by Suppressing the Expression of Long Non-coding RNA TCONS-00026762

2021 ◽  
Vol 12 ◽  
Author(s):  
Xing Liu ◽  
Pingsheng Zhou ◽  
Keqing He ◽  
Zhili Wen ◽  
Yong Gao
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Cell Lines ◽  
Function Analysis ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
Hcc Cells

Background: The etiology and carcinogenesis of hepatocellular carcinoma (HCC) are associated with various risk factors. Saponins extracted from Dioscorea zingiberensis C. H. Wright exhibit antitumor activity against HCC. This study aimed to investigate the effect and the underlying mechanism of Dioscorea Zingiberensis new saponin (ZnS) on HCC.Methods: Human HCC cell lines, Huh7 and SMMC-7721, were treated with different concentrations of ZnS. Cell apoptosis was determined via flow cytometry assay. Differentially expressed lncRNAs (DElncRNAs) in ZnS-treated SMMC-7721 cells were determined through RNA-sequence. The role of lncRNA TCONS-00026762 in HCC was investigated gain of function analysis, along with cell proliferation, apoptosis, and invasion in HCC cells. A subcutaneous xenograft of SMMC-7721 cell lines was established to study the effects of TCONS-00026762 in vivo. The expression of apoptosis-related proteins was detected in vivo and in vitro via western blotting.Results: ZnS inhibited the proliferation of HCC cell in a dose-dependent manner. ZnS could induce apoptosis in HCC cells. Illumina sequencing results showed that 493 DElncRNAs were identified in ZnS-treated SMMC-7721 cells. TCONS-00026762 expression was down-regulated in the ZnS-treated SMMC-7721 cells. TCONS-00026762 inhibited the effect of ZnS on the proliferation, apoptosis, and invasion of HCC cells. ZnS inhibited the tumor growth, while, TCONS-00026762 promoted tumor growth in vivo. Furthermore, ZnS and TCONS-00026762 regulated cell apoptotic pathways.Conclusion: ZnS significantly inhibits the viability, apoptosis, invasion, and tumorigenicity of HCC cells by regulating the expression of TCONS-00026,762. Our findings provide novel insights into the potential role of lncRNA in HCC therapy.

scholarly journals Modulation of SIRT3 expression through CDK4/6 enhances the anti-cancer effect of sorafenib in hepatocellular carcinoma cells

2020 ◽  
Author(s):  
HanHee Jo ◽  
Yusun Park ◽  
Taehun Kim ◽  
Jisu Kim ◽  
JongSook Lee ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Combined Treatment ◽  
Xenograft Model ◽  
Cancer Tissue ◽  
Sorafenib Treatment ◽  
Tumor Types ◽  
Related Proteins ◽  
Sirt3 Expression ◽  
Hcc Cells

Abstract Background : Hepatocellular carcinoma (HCC) is the leading cause of cancer-related deaths worldwide. The only drug currently approved for clinical use in the treatment of advanced HCC is sorafenib. However, many patients with HCC show reduced sensitivity to sorafenib during treatment. SIRT3, a member of the mammalian sirtuin family, is a tumor suppressor in certain tumor types. However, only few studies have investigated the effects of SIRT3 on tumor prognosis and sorafenib sensitivity in patients with HCC. Here, we aimed to investigate the correlation between SIRT3 expression and glucose metabolism and proliferation in HCC and discover effective compounds that increase endogenous SIRT3 modulation effect of sorafenib. Methods: To determine the correlation between SIRT3 and glucose related proteins, immunostaining was performed with liver cancer tissue using various antibodies. To investigate whether the expression of SIRT3 in HCC is related to the resistance to sorafenib, we treated sorafenib after the modulation of SIRT3 levels in HCC cell lines (overexpression in Huh7, knockdown in HepG2). We also employed PD0332991 to modulate the SIRT3 expression in HCC cell and conducted functional assays. Results: SIRT3 expression was downregulated in high glycolytic and proliferative HCC cells of human patients, xenograft model and HCC cell lines. Moreover, SIRT3 expression was downregulated after sorafenib treatment, resulting in reduced drug sensitivity in HCC cell lines. To enhance the anti-tumor effect of sorafenib, we employed PD0332991 (CDK4/6-Rb inhibitor) based on the correlation between SIRT3 and phosphorylated retinoblastoma protein in HCC. Notably, combined treatment with sorafenib and PD0332991 showed an enhancement of the anti-tumor effect in HCC cells. Conclusions: Our data suggest that the modulation of SIRT3 by CDK4/6 inhibition might be useful for HCC therapy together with sorafenib, which, unfortunately, has limited efficacy and whose use is often associated with drug resistance.

scholarly journals A Novelty of Long Non-coding RNA LOXL1-AS1: Suppresses Tumor Progression and Metastasis and an Independent Favorable Prognostic Factor in Hepatocellular Carcinoma

2021 ◽  
Author(s):  
Maher Hendi ◽  
Yu Pan ◽  
Gyabaah Owusu-Ansah Kwabena ◽  
Bin Zhang ◽  
Yifan Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Clinical Results ◽  
Second Primary ◽  
Malignant Liver Tumor ◽  
Term Survival ◽  
Potential Biomarker ◽  
Hcc Cells

Abstract Background: Hepatocellular Carcinoma (HCC) is the second primary causes of cancer death globally, And the sixth mostly common malignant liver tumor with poor clinical results. The long term survival of HCC patients was effected and influenced by the low rate of early diagnosis and high risk of recurrence and metastasis in post operative .Although the survival of HCC patients had improved due to improved diagnosis, In Addition Increasing amount of long non-coding RNAs (lncRNAs) have been revealed to be implicated in the carcinogenesis and progression of HCC. The potential role of Loxl1-As1 in the progression and metastasis of HCC is still not clear and needs exploring and more researching.Methods: By using a lncRNA microarray, we identified a novelty of lncRNA Loxl1-As1 .The expression of lncRNA high downregulated in metastatic HCC (Loxl1-As1) in cell lines and tissues was detected by quantitative real-time PCR (qRT-PCR) and in situ hybridization (ISH).and CCK-8, colony formation and flow cytometry were performed to investigate the role of Loxl1-As1 in HCC cell proliferation, cell cycle and apoptosis in vitro and migration were investigated in HCC cell lines bot in vitro, Western blot was used to detect the downstream of Loxl1-As1.Results: Clinically investigation,Loxl1-As1 correlated with good and favorable prognosis of HCC patients. and Loxl1-As1 was down-regulated in HCC tissues and cell lines. The ISH assay revealed that Loxl1-As1 expression was significantly decreased in 177 paraffin-embedded samples from patients with HCC compared with Non-tumor tissues (adjacent tissues )and Loxl1-as1 expression directly correlated with patient prognosis. In vitro studies indicated that Loxl1-as1 promoted HCC cells’ proliferation and clonogenicity, the expression of Loxl1-as1 suppressed the growth, migration, and metastasis of HCC cells in vitro .Conclusions: Collectively, Our findings reveal a novelty Loxl1-As1for HCC progression and these study demonstrated that Loxl1-As1, overexpressed in HCC and associated with good prognosis , and it’s an important role in the progression and metastasis of HCC. Finally we suggest that lncRNA Loxl1-As1 might be a potential biomarker and therapeutic target for HCC,

scholarly journals Role of tight junction-associated MARVEL protein marvelD3 in migration and Epithelial–Mesenchymal Transition of hepatocellular carcinoma

2021 ◽  
Author(s):  
Yanmeng Li ◽  
Teng Li ◽  
Donghu Zhou ◽  
Jia Wei ◽  
Zhenkun Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tight Junction ◽  
Tumor Cell ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Related Proteins ◽  
Hcc Cells

Abstract BackgroundTight junction (TJ) imbalance is associated with hepatocellular carcinoma (HCC). MarvelD3, which contains a conserved MARVEL (MAL and related proteins for vesicle trafficking and membrane link) domain similarly to occludin and tricellulin, is a recently identified integral membrane protein that forms TJs. However, little is known about the possible roles of marvelD3 in epithelial–mesenchymal transition (EMT) and metastasis of HCC. We aimed to demonstrate the role of marvelD3 in inhibiting HCC EMT and migration and further explore the underlying molecular mechanisms.MethodsMarvlD3 expression was assessed in HCC and normal liver tissues. Changes in marvelD3 expression were analyzed during transforming growth factor β1 (TGF-β1) and snail/slug-induced EMT. MarvelD3 knockdown HCC cell lines were established using marvelD3-siRNA to analyze correlations between marvelD3 and EMT-related proteins. Tumor cell behaviors were analyzed in marvelD3 knockdown HCC cells. Associations between marvelD3 and genes in the nuclear factor (NF)-κB pathway were also analyzed.ResultsLoss of marvelD3 expression was significantly correlated with the occurrence and TNM stage of HCC. MarvelD3 was downregulated in HCC cells with TGF-β and snail/slug-induced EMT. Expression of marvelD3 protein was significantly associated with E-cadherin and vimentin in HCC cell lines. Knockdown of marvelD3 promoted tumor cell migration concomitant with activation of the NF-κB signaling pathway and increased matrix metallopeptidase 9 expression.ConclusionsOur study demonstrated that MarvelD3 inhibited EMT and migration of HCC cells via NF-κB signaling pathway. This suggests that marvelD3 is a novel potential biomarker for the treatment and prognosis of HCC.

scholarly journals Identification of PAFAH1B3 as Candidate Prognosis Marker and Potential Therapeutic Target for Hepatocellular Carcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Weikang Xu ◽  
Xinyu Lu ◽  
Jing Liu ◽  
Qianhui Chen ◽  
Xuan Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Lines ◽  
Critical Role ◽  
Disease Free Survival ◽  
The Cancer Genome Atlas ◽  
Transwell Assay ◽  
Mutational Status ◽  
Prognosis Marker ◽  
Hcc Cells

BackgroundHepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related deaths worldwide. PAFAH1B3 plays an important role on occurrence and development in a variety tumor. However, the function of PAFAH1B3 in HCC remains unclear.MethodsThe TIMER, ONCOMINE, Human Protein Atlas (HPA), GEPIA, The Cancer Genome Atlas (TCGA), HCCDB, UALCAN and LinkedOmics database were used to analyze the prognostic value, co-expression genes and regulator networks of PAFAH1B3 in HCC. siRNA transfections and inhibitor of PAFAH1B3 P11 were used to verify the anti-tumor effect on HCC cell lines. Gene expression was detected by qRT-PCR. The functions of PAFAH1B3 downregulation in HCC cell lines were investigated using cell cycle analysis, apoptosis detection, CCK8 assay and transwell assay. Western blot was used to evaluate the role of PAFAH1B3 on metabolic pathways in HCC cells.ResultsBased on the data from databases, the expression of PAFAH1B3 was remarkably increased in HCC patients. High expression of PAFAH1B3 was associated with poorer overall survival (OS) and disease-free survival (DFS). And PAFAH1B3 was notably linked to age, sex, grade, stage, race, and TP53 mutational status. Then, the functional network analysis showed PAFAH1B3 may be involved in HCC through cell cycle, cell metabolism, spliceosome, and RNA transport. Furthermore, the mRNA expression of PAFAH1B3 was also increased in HCC cell lines. Flow cytometry analysis showed that PAFAH1B3 manipulated apoptosis and cell cycle regulation. CCK8 assay showed that PAFAH1B3 silencing or pharmacologic inhibitor of PAFAH1B3 inhibited the proliferation of HepG2, Huh7 and MHCC-97H cells. Transwell assay results showed that PAFAH1B3 silencing also significantly impaired the invasion and migratory ability of HCC cells. In addition, PAFAH1B3 silencing significantly downregulated the expression of glycolysis and lipid synthesis signaling pathways.ConclusionOur findings suggested that PAFAH1B3 plays a critical role in progression of HCC. PAFAH1B3 as a prognosis marker and potential target for HCC has prospective clinical significance.

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