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Keywords {🔍}

prim, hcc, expression, cells, fig, ubec, article, signaling, genes, patients, tcga, hepg, cell, mhcch, group, dna, tumor, samples, google, scholar, sorafenib, hepatocellular, carcinoma, datasets, overexpression, analysis, cancer, icgc, survival, usa, gene, nantong, dataset, cas, data, growth, gse, ubiquitination, study, protein, proliferation, enrichment, tissues, significantly, enhanced, cases, primase, performed, spheroids, aggressive,

Topics {✒️}

kd-ube2c/ptsb-sh-copgfp-2a-puro plasmids pex4 egfp/t2a/kan/neo oe-ube2c/ptsb02-gfp-puro plasmids org/packages/release/bioc/html/preprocesscore org/packages/release/bioc/html/limma org/web/packages/survival/index activating pi3k/akt/mtor signaling anti-rabbit ig-ip beads regulate pi3k-akt-mtor partially pi3k/akt/mtor signaling markers activating akt/mtor signaling pi3k/akt/mtor signaling dna-dependent rna polymerases hbv-related hepatocellular carcinoma modulating akt/mtor signaling common post-transcriptional modification crucial post-translational modification log-rank test p-values vital tumor-suppressive signaling promoting epithelial-mesenchymal transition prim1 de-stabilized p53 cancer genome atlas promotes epithelial-mesenchymal transition article download pdf ubiquitin-conjugating enzyme priori-defined gene sets hepg2-derived spheroids model protease inhibitor boriezomib upper chambers pre-coated ube2c-mediated p53 inactivation prim1-mediated p53 ubiquitination full access ube2c-mediated p53 ubiquitination prim1-silenced mhcc97h cells mhcc97h-derived xenograft tumors protein half-life assay hcc cells-derived spheroids ubiquitin mediated proteolysis tumor-related biological processes human dna primase dna damage checkpoint akt/mtor signaling p53 tumor-suppressor function induced dna damage ube2c-mediated p53 degradation privacy choices/manage cookies 5 × 106/100  μl serum-free dmem normalized enrichment score ubiquitination-dependent manner oe-prim1 plasmid

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         headline:DNA primase subunit 1 deteriorated progression of hepatocellular carcinoma by activating AKT/mTOR signaling and UBE2C-mediated P53 ubiquitination
         description: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. 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. 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. 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.
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            AKT/mTOR
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      headline:DNA primase subunit 1 deteriorated progression of hepatocellular carcinoma by activating AKT/mTOR signaling and UBE2C-mediated P53 ubiquitination
      description: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. 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. 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. 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.
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         DNA primase subunit 1
         Hepatocellular carcinoma
         P53
         AKT/mTOR
         Molecular target
         Cell Biology
         Microbiology
         Stem Cells
         Neurobiology
         Proteomics
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               type:PostalAddress
            type:Organization
      name:Hua Huang
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      name:Li You
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      name:Jianping Zhang
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      name:Jie Zhang
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      name:Chun Cheng
      affiliation:
            name:Nantong University
            address:
               name:School of Medicine, Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      name:Wenkai Ni
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Wenjie Zheng
      url:http://orcid.org/0000-0002-3073-4596
      affiliation:
            name:Affiliated Hospital of Nantong University
            address:
               name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
            name:Affiliated Hospital of Nantong University
            address:
               name:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:School of Medicine, Nantong University, Nantong, China
      name:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:School of Medicine, Nantong University, Nantong, China
      name:Department of Radiology, Wake Forest School of Medicine, One Medical Center Boulevard, Winston-Salem, USA
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, China
      name:School of Medicine, Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China
      name:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, China

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