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We are analyzing https://link.springer.com/article/10.1007/s10238-021-00742-8.

Title:
RMI2 is a prognostic biomarker and promotes tumor growth in hepatocellular carcinoma | Clinical and Experimental Medicine
Description:
Genomic instability is a hallmark of all cancers. RMI2 is a crucial component of the BLM-TopoIIIa-RMI1-RMI2 complex that maintains genome stability. It has been shown to accelerate tumor progression in lung cancer, cervical cancer, and prostate cancer. However, its expression and function in hepatocellular carcinoma (HCC) remain poorly defined. In this study, gene expression data and corresponding clinical information of HCC were downloaded from the TCGA, ICGC, and GEO databases. The expression level and clinical significance of RMI2 in HCC were then analyzed. In addition, cellular and molecular biology experiments were conducted to explore the effects of silencing and overexpression of RMI2 on human liver cancer cells and the associated mechanisms. The results showed that RMI2 expression was elevated in HCC tissues. High expression of RMI2 was correlated with shorter survival and poor prognosis of patients. The results of CCK-8, Edu, and clonogenic assays confirmed that RMI2 overexpression promoted the proliferation of HCC cells. Flow cytometric analysis demonstrated that RMI2 overexpression enhanced G1-S phase transition and decreased apoptosis. Moreover, the protein expression of key effector molecules in the p53 signaling pathway was reduced following RMI2 overexpression. In summary, these results indicate that RMI2 promotes the growth of HCC cells and suppresses their apoptosis by inhibiting the p53 signaling pathway. This study provides new insights into the mechanisms driving HCC tumorigenesis and new therapeutic targets.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,932 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We can't figure out the monetization strategy.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

article, google, scholar, cas, carcinoma, cancer, hepatocellular, rmi, cell, nat, rev, expression, hcc, data, liu, access, privacy, cookies, content, information, tumor, growth, complex, study, res, analysis, publish, search, clinical, prognostic, promotes, july, zhang, instability, genome, overexpression, liver, mechanisms, signaling, pathway, therapy, author, clin, dis, sorafenib, springer, log, journal, research, experimental,

Topics {βœ’οΈ}

topo iiiΞ±-rmi1-rmi2 complex blm-topoiiia-rmi1-rmi2 complex month download article/chapter pro-apoptotic sorafenib signaling synergistic anti-tumor activity molecular biology experiments dna helicase rtel1 dig liver dis p53 signaling pathway full article pdf privacy choices/manage cookies efficient cancer therapy nat rev cancer blm-dependent pathway hepatocellular carcinoma subclass hepatocellular carcinoma unresponsive related subjects integrated bioinformatic analysis promotes tumor growth experimental medicine aims regulate p53 activity annu rev pathol prognostic biomarkers cell death dis cell cycle proteins cancer genome instability cyclin-dependent kinase 2 cyclind1/cdk4 complex genome sequencing studies gene expression data clin cancer res european economic area remain poorly defined clonogenic assays confirmed da fonseca lg nucleic acids res tumour evolution 45s rdna repeats malignant solid tumors murine hepatocytes depends neuroendocrine prostate cancer conditions privacy policy socs1 blocks g1 targeting mutant p53 cell cycle transition key effector molecules rmi2 overexpression promoted ximing xu article li check access

Schema {πŸ—ΊοΈ}

WebPage:
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         description:Genomic instability is a hallmark of all cancers. RMI2 is a crucial component of the BLM-TopoIIIa-RMI1-RMI2 complex that maintains genome stability. It has been shown to accelerate tumor progression in lung cancer, cervical cancer, and prostate cancer. However, its expression and function in hepatocellular carcinoma (HCC) remain poorly defined. In this study, gene expression data and corresponding clinical information of HCC were downloaded from the TCGA, ICGC, and GEO databases. The expression level and clinical significance of RMI2 in HCC were then analyzed. In addition, cellular and molecular biology experiments were conducted to explore the effects of silencing and overexpression of RMI2 on human liver cancer cells and the associated mechanisms. The results showed that RMI2 expression was elevated in HCC tissues. High expression of RMI2 was correlated with shorter survival and poor prognosis of patients. The results of CCK-8, Edu, and clonogenic assays confirmed that RMI2 overexpression promoted the proliferation of HCC cells. Flow cytometric analysis demonstrated that RMI2 overexpression enhanced G1-S phase transition and decreased apoptosis. Moreover, the protein expression of key effector molecules in the p53 signaling pathway was reduced following RMI2 overexpression. In summary, these results indicate that RMI2 promotes the growth of HCC cells and suppresses their apoptosis by inhibiting the p53 signaling pathway. This study provides new insights into the mechanisms driving HCC tumorigenesis and new therapeutic targets.
         datePublished:2021-07-18T00:00:00Z
         dateModified:2021-07-18T00:00:00Z
         pageStart:229
         pageEnd:243
         sameAs:https://doi.org/10.1007/s10238-021-00742-8
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            Hepatocellular carcinoma
            Prognosis
            Growth
            p53
            Internal Medicine
            Hematology
            Oncology
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      headline:RMI2 is a prognostic biomarker and promotes tumor growth in hepatocellular carcinoma
      description:Genomic instability is a hallmark of all cancers. RMI2 is a crucial component of the BLM-TopoIIIa-RMI1-RMI2 complex that maintains genome stability. It has been shown to accelerate tumor progression in lung cancer, cervical cancer, and prostate cancer. However, its expression and function in hepatocellular carcinoma (HCC) remain poorly defined. In this study, gene expression data and corresponding clinical information of HCC were downloaded from the TCGA, ICGC, and GEO databases. The expression level and clinical significance of RMI2 in HCC were then analyzed. In addition, cellular and molecular biology experiments were conducted to explore the effects of silencing and overexpression of RMI2 on human liver cancer cells and the associated mechanisms. The results showed that RMI2 expression was elevated in HCC tissues. High expression of RMI2 was correlated with shorter survival and poor prognosis of patients. The results of CCK-8, Edu, and clonogenic assays confirmed that RMI2 overexpression promoted the proliferation of HCC cells. Flow cytometric analysis demonstrated that RMI2 overexpression enhanced G1-S phase transition and decreased apoptosis. Moreover, the protein expression of key effector molecules in the p53 signaling pathway was reduced following RMI2 overexpression. In summary, these results indicate that RMI2 promotes the growth of HCC cells and suppresses their apoptosis by inhibiting the p53 signaling pathway. This study provides new insights into the mechanisms driving HCC tumorigenesis and new therapeutic targets.
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      dateModified:2021-07-18T00:00:00Z
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         Prognosis
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         Internal Medicine
         Hematology
         Oncology
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               name:Cancer Center, Renmin Hospital of Wuhan University, Wuhan, China
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External Links {πŸ”—}(111)

Analytics and Tracking {πŸ“Š}

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