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  • 1
    Online Resource
    Online Resource
    Ubiquitin-specific protease 7 is a drug-able target that promotes hepatocellular carcinoma and chemoresistance
    Springer Science and Business Media LLC ; 2020
    In:  Cancer Cell International Vol. 20, No. 1 ( 2020-12)
    Details
    In: Cancer Cell International, Springer Science and Business Media LLC, Vol. 20, No. 1 ( 2020-12)
    Abstract: Ubiquitin-specific protease 7 (USP7) is a de-ubiquitin enzyme that plays an essential role in multiple cancers and becomes a target for treatment. However, the role of USP7 and its therapeutic value for HCC remains unclear. Methods USP7 expression was examined in HCC tissues by western blot and immunohistochemistry. The correlation of USP7 and HCC prognosis was analyzed by Kaplan–Meier survival method. Mass spectrometry was determined and cell proliferation and tumorigenicity assays were conducted in vitro and in vivo treated by P22077 and sgRNA-USP7. Results USP7 expression was significantly increased in HCC and associated with its progression. Interestingly, many HCC cells are sensitive to USP7 inhibition by using P22077. P22077 treatment not only induced cell death but also inhibited cell proliferation and migration in Huh7 and SK-Hep1 cells. In a xenograft model, P22077 efficiently inhibited tumor growth. In chemo-resistant HCC cells, P22077 decreased cell sensitivity to chemotherapy. In addition, mass spectrometry reveals 224 of significantly changed proteins upon P22077 treatment. Conclusions We demonstrate a critical role of USP7 in HCC devolvement and chemoresistance. Disruption of USP7 function results in dis-regulated several key biological processes and subsequently activates BAX. USP7 might be a novel and drug-able target in HCC.
    Type of Medium: Online Resource
    ISSN: 1475-2867
    URL: Article
    DOI: 10.1186/s12935-020-1109-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2091573-1
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  • 2
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    DNA primase subunit 1 deteriorated progression of hepatocellular carcinoma by activating AKT/mTOR signaling and UBE2C-mediated P53 ubiquitination
    Springer Science and Business Media LLC ; 2021
    In:  Cell & Bioscience Vol. 11, No. 1 ( 2021-12)
    Details
    In: Cell & Bioscience, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2021-12)
    Abstract: DNA primase subunit 1 (PRIM1) has been reported as a novel oncogene in several cancer types. However, its roles in hepatocellular carcinoma (HCC) remain unclear. This study aimed to investigate underlying mechanisms of PRIM1 and identify it as a potential molecular target for HCC. Methods Hub genes were screened between HCC tissues and normal liver tissues in 3 gene expression omnibus (GEO) datasets and the cancer genome atlas (TCGA). The expression features and prognostic value of one of the hub genes PRIM1 were analyzed by bioinformatic analyses and immunohistochemistry. Loss-of-function and gain-of-function studies were used to investigate the regulatory role of PRIM1 in HCC cells. Real-time (RT)-qPCR, western blotting, and ubiquitin immunoprecipitation assays were performed to explore the underlying mechanisms. The xenograft model was employed to detect the roles of PRIM1 in tumor growth in vivo. Finally, the 3D spheroid model was conducted to validate the role of PRIM1 in tumor growth and sorafenib resistance. Results The hub genes of HCC were screened in multiple bioinformatic datasets. PRIM1, as one of the hub genes, was significantly overexpressed in HCC tissues in mRNA and protein levels. In addition, high expression of PRIM1 indicated poor prognosis of HCC patients in TCGA, ICGC, and Nantong cohorts. Overexpression of PRIM1 promoted the proliferation, migration/invasion, and sorafenib resistance of HCC cells, with the decrease in apoptosis and cell cycle arrest. Mechanically, PRIM1 facilitated epithelial-mesenchymal transition (EMT) process and the activity of PI3K/AKT/mTOR signaling of HCC cells. Additionally, PRIM1 could cause the ubiquitination and degradation of P53 by upregulating Ubiquitin Conjugating Enzyme E2 C (UBE2C). Furthermore, knockdown of PRIM1 significantly inhibited the growth of xenograft tumors and HCC cells-derived spheroids with enhanced sorafenib resistance. Conclusion This study implies that PRIM1 may play a key role in the progression of HCC and may serve as a potential target for HCC treatment.
    Type of Medium: Online Resource
    ISSN: 2045-3701
    URL: Article
    DOI: 10.1186/s13578-021-00555-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2593367-X
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  • 3
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    Image_1.PDF
    Frontiers Media SA ; 2020
    In:  Frontiers in Molecular Biosciences Vol. 7 ( 2020-12-10)
    Details
    In: Frontiers in Molecular Biosciences, Frontiers Media SA, Vol. 7 ( 2020-12-10)
    Abstract: Purpose: N6-methyladenosine (m 6 A) RNA methylation has been implicated in various malignancies. This study aimed to identify the m 6 A 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 m 6 A RNA methylation regulators was correlated with malignant clinicopathological characteristics of HCC patients. The Cox regression and LASSO analyses identified a risk signature with five m 6 A 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 m 6 A RNA methylation regulators for HCC prognosis. In addition, YTHDF1 was a potential molecular target for HCC treatment.
    Type of Medium: Online Resource
    ISSN: 2296-889X
    URL: Article
    URL: Article
    DOI: 10.3389/fmolb.2020.604766
    DOI: 10.3389/fmolb.2020.604766.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2814330-9
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  • 4
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    Biological testing of chitosan‐collagen‐based porous scaffolds loaded with PLGA/Triamcinolone microspheres for ameliorating endoscopic dissection‐related stenosis in oesophagus
    Wiley ; 2021
    In:  Cell Proliferation Vol. 54, No. 3 ( 2021-03)
    Details
    In: Cell Proliferation, Wiley, Vol. 54, No. 3 ( 2021-03)
    Abstract: Endoscopic submucosal dissection (ESD), a preferential approach for early oesophageal neoplasms, inevitably results in oesophageal strictures in patients. Clinical use of glucocorticoids through submucosal injection is beneficial for inhibiting oesophageal stricture following injury; however, it also has limitations, such as dose loss and perforation. Hence, alternatives to glucocorticoid therapy should be developed. Methods A novel porous composite scaffold, ChCo‐TAMS, composed of chitosan, collagen‐I and triamcinolone acetonide (TA) loaded into poly (lactic‐co‐glycolic) acid (PLGA) microspheres (TAMS), was successfully constructed and subjected to biological testing to ameliorate oesophageal ESD‐related stenosis. Results The synthesized biomaterials displayed unique properties in inhibiting the activation of macrophages, chemokine‐mediated cell recruitment and fibrogenesis of fibroblasts. Further application of the scaffolds in the rat dermal defect and porcine oesophageal ESD model showed that these novel scaffolds played a robust role in inhibiting wound contracture and oesophageal ESD strictures. Conclusions The developed composite scaffolds provide a promising clinical medical device for the prevention of post‐operative oesophageal stricture.
    Type of Medium: Online Resource
    ISSN: 0960-7722 , 1365-2184
    URL: Issue
    URL: Article
    DOI: 10.1111/cpr.v54.3
    DOI: 10.1111/cpr.13004
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2019986-7
    SSG: 12
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  • 5
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    Placenta mesenchymal stem cell-derived extracellular vesicles alleviate liver fibrosis by inactivating hepatic stellate cells through a miR-378c/SKP2 axis
    Springer Science and Business Media LLC ; 2023
    In:  Inflammation and Regeneration Vol. 43, No. 1 ( 2023-10-05)
    Details
    In: Inflammation and Regeneration, Springer Science and Business Media LLC, Vol. 43, No. 1 ( 2023-10-05)
    Abstract: Extracellular vesicles derived from mesenchymal stem/stromal cells (MSCs) have shown therapeutic effects on liver fibrosis. This study aimed to evaluate the effects of extracellular vesicles from placenta-derived MSCs (Pd-MSCs-EVs) on liver fibrosis at 3D/2D levels and explore the potential mechanisms. Methods The multicellular liver organoids, consisting of hepatocytes, hepatic stellate cells (HSCs), Kupffer cells, and liver sinusoidal endothelial cells, were observed for growth status, morphological changes, and metabolism. Human transformation growth factor- beta 1 (TGF-β1) was used to induce fibrosis at optimal concentration. The anti-fibrosis effects of Pd-MSCs-EVs were evaluated in liver organoids and HSCs models. Anti-fibrotic content of Pd-MSCs-EVs was identified by multiple experimental validations. Results TGF-β1 induced fibrosis in liver organoids, while Pd-MSCs-EVs significantly alleviated fibrotic phenotypes. Following serial verifications, miR-378c was identified as a potential key anti-fibrosis content. In contrast, miR-378c depletion decreased the anti-fibrotic effects of Pd-MSCs-EVs. Additionally, Pd-MSCs-EVs administration repressed TGF-β1-mediated HSCs activation at 2D or 3D levels. Mechanistically, exosomal miR-378c inactivated HSCs by inhibiting epithelial-mesenchymal transition (EMT) through stabilizing E-cadherin via targeting its E3 ubiquitin ligase S-Phase Kinase Associated Protein 2 (SKP2). Conclusion Pd-MSCs-EVs ameliorated TGF-β1-induced fibrosis by deactivating HSCs in a miR-378c/SKP2-dependent manner, which may be an efficient therapeutic candidate for liver fibrosis.
    Type of Medium: Online Resource
    ISSN: 1880-8190
    URL: Article
    DOI: 10.1186/s41232-023-00297-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2411877-1
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  • 6
    Online Resource
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    Flap endonuclease 1 Facilitated Hepatocellular Carcinoma Progression by Enhancing USP7/MDM2-mediated P53 Inactivation
    Ivyspring International Publisher ; 2022
    In:  International Journal of Biological Sciences Vol. 18, No. 3 ( 2022), p. 1022-1038
    Details
    In: International Journal of Biological Sciences, Ivyspring International Publisher, Vol. 18, No. 3 ( 2022), p. 1022-1038
    Type of Medium: Online Resource
    ISSN: 1449-2288
    URL: Article
    DOI: 10.7150/ijbs.68179
    Language: English
    Publisher: Ivyspring International Publisher
    Publication Date: 2022
    detail.hit.zdb_id: 2179208-2
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  • 7
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    Minichromosome maintenance protein family member 6 mediates hepatocellular carcinoma progression by recruiting UBE3A to induce P53 ubiquitination
    Elsevier BV ; 2023
    In:  International Journal of Biological Macromolecules Vol. 248 ( 2023-09), p. 125854-
    Details
    In: International Journal of Biological Macromolecules, Elsevier BV, Vol. 248 ( 2023-09), p. 125854-
    Type of Medium: Online Resource
    ISSN: 0141-8130
    URL: Article
    DOI: 10.1016/j.ijbiomac.2023.125854
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1483284-7
    SSG: 12
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  • 8
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    Circadian gene CSNK1D promoted the progression of hepatocellular carcinoma by activating Wnt/β-catenin pathway via stabilizing Dishevelled Segment Polarity Protein 3
    Springer Science and Business Media LLC ; 2022
    In:  Biological Procedures Online Vol. 24, No. 1 ( 2022-12-02)
    Details
    In: Biological Procedures Online, Springer Science and Business Media LLC, Vol. 24, No. 1 ( 2022-12-02)
    Abstract: A variety of studies have connected circadian rhythm to the initiation and progression of hepatocellular carcinoma (HCC). The purpose of this study was to figure out about the circadian genes' profile characteristics, prognostic significance, and targeted values in HCC. Methods The expression profiles and prognostic significance of circadian genes in the cancer genome atlas liver hepatocellular carcinoma (TCGA-LIHC) database were investigated using bioinformatics analysis. The expression features of Casein Kinase 1 Delta (CSNK1D), a robust signature gene, was further detected by immunohistochemistry, western blotting and Real-time quantitative PCR (RT-qPCR) in a local HCC cohort. The effect of CSNK1D on corresponding phenotypes of HCC cells was evaluated using Cell Counting Kit-8 (CCK8), flowcytometry, clone assay, Transwell assay, and xenograft assay. In addition, the underlying mechanisms of CSNK1D in the Wnt/β-catenin signaling were validated by multiple molecular experiments. Results Abnormal expression of the Circadian genome was associated with the malignant clinicopathological characteristics of HCC patients. A 10 circadian gene-based signature with substantial prognostic significance was developed using Cox regression and least absolute shrinkage and selection operator (LASSO) analysis. Of them, CSNK1D, significantly elevated in a local HCC cohort, was chosen for further investigation. Silencing or overexpression of CSNK1D significantly reduced or increased proliferation, invasion, sorafenib resistance, xenograft development, and epithelial-mesenchymal transformation (EMT) of HCC cells, respectively. Mechanically, CSNK1D exacerbated the aggressiveness of HCC cells by activating Wnt/β-catenin signaling through interacting with Dishevelled Segment Polarity Protein 3 (DVL3). Conclusions The Circadian gene CSNK1D was found to contribute to HCC progression by boosting the Wnt/β-catenin pathway, hinting that it could be a prospective therapeutic target for HCC.
    Type of Medium: Online Resource
    ISSN: 1480-9222
    URL: Article
    DOI: 10.1186/s12575-022-00183-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2027823-8
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  • 9
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    The lncRNA B3GALT5-AS1 Functions as an HCC Suppressor by Regulating the miR-934/UFM1 Axis
    Hindawi Limited ; 2021
    In:  Journal of Oncology Vol. 2021 ( 2021-10-20), p. 1-18
    Details
    In: Journal of Oncology, Hindawi Limited, Vol. 2021 ( 2021-10-20), p. 1-18
    Abstract: Accumulating evidence has demonstrated that long noncoding RNA (lncRNA) is importantly related to the occurrence and development of cancer. According to reports, the expression of B3GALT5-AS1 in hepatocellular carcinoma (HCC) is downregulated; however, the role of B3GALT5-AS1 in HCC is not yet clear. In this study, our purpose is to explore the biological function of B3GALT5-AS1 in HCC and its coupling mechanism with miR-934 and ubiquitin-fold modifier 1 (UFM1). We found that the B3GALT5-AS1 expression level was of significant reduction in both HCC tissues and cell lines; B3GALT5-AS1 overexpression (ov) may inhibit the malignant features of HCC. In addition, we demonstrated that miR-934 mimics could reverse the effect of B3GALT5-AS1 ov, which proved miR-934 was the downstream regulator of B3GALT5-AS1. Furthermore, si-UFM1 could reverse the effect of miR-934 inhibitor, which revealed the connection between them. Moreover, we found that B3GALT5-AS1 could keep down the PI3K/AKT pathway through UFM1. Our results demonstrated that B3GALT5-AS1 was an excellent HCC suppressant by regulating miR-934 and UFM1 to achieve negative regulation of HCC cell proliferation, invasion, and metastasis, indicating that B3GALT5-AS1 is a promising potential therapeutic target for HCC treatment.
    Type of Medium: Online Resource
    ISSN: 1687-8469 , 1687-8450
    URL: Article
    DOI: 10.1155/2021/1776432
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2461349-6
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  • 10
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    Presentation_1.pdf
    Frontiers Media SA ; 2021
    In:  Frontiers in Oncology Vol. 11 ( 2021-2-25)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 11 ( 2021-2-25)
    Abstract: Ubiquitin-specific proteases (USPs), as a sub-family of deubiquitinating enzymes (DUBs), are responsible for the elimination of ubiquitin-triggered modification. USPs are recently correlated with various malignancies. However, the expression features and clinical significance of USPs have not been systematically investigated in hepatocellular carcinoma (HCC). Methods Genomic alterations and expression profiles of USPs were investigated in CbioPortal and The Cancer Genome Atlas (TCGA) Liver hepatocellular carcinoma (LIHC) dataset. Cox regression and least absolute shrinkage and selection operator (LASSO) analyses were conducted to establish a risk signature for HCC prognosis in TCGA LIHC cohort. Subsequently, Kaplan-Meier analysis, receiver operating characteristic (ROC) curves and univariate/multivariate analyses were performed to evaluate the prognostic significance of the risk signature in TCGA LIHC and international cancer genome consortium (ICGC) cohorts. Furthermore, we explored the alterations of the signature genes during hepatocarcinogenesis and HCC progression in GSE89377. In addition, the expression feature of USP39 was further explored in HCC tissues by performing western blotting and immunohistochemistry. Results Genomic alterations and overexpression of USPs were observed in HCC tissues. The consensus analysis indicated that the USPs-overexpressed sub-Cluster was correlated with aggressive characteristics and poor prognosis. Cox regression with LASSO algorithm identified a risk signature formed by eight USPs for HCC prognosis. High-risk group stratified by the signature score was correlated with advanced tumor stage and poor survival HCC patients in TCGA LIHC cohort. In addition, the 8-USPs based signature could also robustly predict overall survival of HCC patients in ICGC(LIRI-JP) cohort. Furthermore, gene sets enrichment analysis (GSEA) showed that the high-risk score was associated with tumor-related pathways. According to the observation in GSE89377, USP39 expression was dynamically increased with hepatocarcinogenesis and HCC progression. The overexpression of USP39 was further determined in a local HCC cohort and correlated with poor prognosis. The co-concurrence analysis suggested that USP39 might promote HCC by regulating cell-cycle- and proliferation- related genes. Conclusion The current study provided a USPs-based signature, highlighting its robust prognostic significance and targeted value for HCC treatment.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2021.629327
    DOI: 10.3389/fonc.2021.629327.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2649216-7
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