FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2950685841> ?p ?o ?g. }

• W2950685841 endingPage "5834" @default.
• W2950685841 startingPage "5821" @default.
• W2950685841 abstract "microRNA-548b suppresses aggressive phenotypes of hepatocellular carcinoma by directly targeting high-mobility group box 1 mRNA Zhennan Yun,1 Fanqi Meng,1 Peiqiang Jiang,2 Meng Yue,1 Shiquan Li11Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, People’s Republic of China; 2Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, People’s Republic of ChinaBackground and purpose: An increasing number of studies have revealed that microRNAs (miRNAs) are the main drivers of hepatocarcinogenesis including progression to later stages of liver cancer. Recently, miR-548b was identified as a cancer-related miRNA in glioma and tongue squamous cell carcinoma. Nonetheless, the expression pattern and specific roles of miR-548b in hepatocellular carcinoma (HCC) have not yet been clarified.Methods: Expression levels of miR-548b in HCC tissues and cell lines were measured by reverse-transcription quantitative PCR. In vitro and in vivo functional assays were performed to determine the effects of miR-548b on the malignant phenotypes of HCC cells. In addition, the molecular mechanisms by which miR-548b regulates the initiation and progression of HCC were investigated in detail.Results: miR-548b expression was weak in HCC tissues and cell lines. The low miR-548b expression significantly correlated with tumor size, TNM stage, and venous infiltration of HCC. In addition, exogenous miR-548b expression suppressed HCC cell proliferation, colony formation, and metastasis and induced apoptosis in vitro. Silencing of miR-548b exerted an opposite effect on these characteristics of HCC cells. Furthermore, miR-548b overexpression hindered tumor growth in vivo. Mechanistic analysis identified high-mobility group box 1 (HMGB1) as a direct target gene of miR-548b in HCC cells. Moreover, an HMGB1 knockdown reproduced the effects of miR-548b upregulation on HCC cells. Recovered HMGB1 expression reversed the effects of miR-548b on HCC cells. Notably, miR-548b overexpression deactivated the PI3K–AKT pathway in HCC cells in vitro and in vivo.Conclusion: Our findings provide the first evidence that miR-548b restrains HCC progression, at least partially, by downregulating HMGB1 and deactivating the PI3K–AKT pathway. Thus, miR-548b might be a novel target for the development of new therapies for HCC.Keywords: microRNA-548b, hepatocellular carcinoma, PI3K–AKT pathway, high-mobility group box 1, HMGB1" @default.
• W2950685841 created "2019-06-27" @default.
• W2950685841 creator A5011506864 @default.
• W2950685841 creator A5014664891 @default.
• W2950685841 creator A5035412780 @default.
• W2950685841 creator A5052104343 @default.
• W2950685841 creator A5082279217 @default.
• W2950685841 date "2019-06-01" @default.
• W2950685841 modified "2023-09-25" @default.
• W2950685841 title "<p>microRNA-548b suppresses aggressive phenotypes of hepatocellular carcinoma by directly targeting high-mobility group box 1 mRNA</p>" @default.
• W2950685841 cites W144423133 @default.
• W2950685841 cites W1513564715 @default.
• W2950685841 cites W1594054294 @default.
• W2950685841 cites W1726906347 @default.
• W2950685841 cites W1887486588 @default.
• W2950685841 cites W1946209449 @default.
• W2950685841 cites W1974285030 @default.
• W2950685841 cites W1976560589 @default.
• W2950685841 cites W1980885318 @default.
• W2950685841 cites W1992082488 @default.
• W2950685841 cites W1996061474 @default.
• W2950685841 cites W2005383307 @default.
• W2950685841 cites W2014946489 @default.
• W2950685841 cites W2019300863 @default.
• W2950685841 cites W2022224233 @default.
• W2950685841 cites W2025575974 @default.
• W2950685841 cites W2038972133 @default.
• W2950685841 cites W2041424679 @default.
• W2950685841 cites W2059133069 @default.
• W2950685841 cites W2079818163 @default.
• W2950685841 cites W2091576301 @default.
• W2950685841 cites W2093073599 @default.
• W2950685841 cites W2104389740 @default.
• W2950685841 cites W2137052325 @default.
• W2950685841 cites W2145457154 @default.
• W2950685841 cites W2160902858 @default.
• W2950685841 cites W2323922475 @default.
• W2950685841 cites W2413711134 @default.
• W2950685841 cites W2525906185 @default.
• W2950685841 cites W2545725900 @default.
• W2950685841 cites W2560292853 @default.
• W2950685841 cites W2624903014 @default.
• W2950685841 cites W2744452424 @default.
• W2950685841 cites W2771889686 @default.
• W2950685841 cites W2781525129 @default.
• W2950685841 cites W2783804618 @default.
• W2950685841 cites W2810167428 @default.
• W2950685841 cites W2844162114 @default.
• W2950685841 cites W2889658717 @default.
• W2950685841 cites W2896031653 @default.
• W2950685841 cites W2900229618 @default.
• W2950685841 cites W2900900388 @default.
• W2950685841 cites W2901568641 @default.
• W2950685841 cites W2901579674 @default.
• W2950685841 cites W2901936812 @default.
• W2950685841 doi "https://doi.org/10.2147/cmar.s198615" @default.
• W2950685841 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6601050" @default.
• W2950685841 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31417317" @default.
• W2950685841 hasPublicationYear "2019" @default.
• W2950685841 type Work @default.
• W2950685841 sameAs 2950685841 @default.
• W2950685841 citedByCount "10" @default.
• W2950685841 countsByYear W29506858412018 @default.
• W2950685841 countsByYear W29506858412020 @default.
• W2950685841 countsByYear W29506858412021 @default.
• W2950685841 countsByYear W29506858412023 @default.
• W2950685841 crossrefType "journal-article" @default.
• W2950685841 hasAuthorship W2950685841A5011506864 @default.
• W2950685841 hasAuthorship W2950685841A5014664891 @default.
• W2950685841 hasAuthorship W2950685841A5035412780 @default.
• W2950685841 hasAuthorship W2950685841A5052104343 @default.
• W2950685841 hasAuthorship W2950685841A5082279217 @default.
• W2950685841 hasBestOaLocation W29506858411 @default.
• W2950685841 hasConcept C104317684 @default.
• W2950685841 hasConcept C119056186 @default.
• W2950685841 hasConcept C121608353 @default.
• W2950685841 hasConcept C126322002 @default.
• W2950685841 hasConcept C127716648 @default.
• W2950685841 hasConcept C143998085 @default.
• W2950685841 hasConcept C145059251 @default.
• W2950685841 hasConcept C1491633281 @default.
• W2950685841 hasConcept C190283241 @default.
• W2950685841 hasConcept C2778019345 @default.
• W2950685841 hasConcept C2779013556 @default.
• W2950685841 hasConcept C502942594 @default.
• W2950685841 hasConcept C54355233 @default.
• W2950685841 hasConcept C62112901 @default.
• W2950685841 hasConcept C71924100 @default.
• W2950685841 hasConcept C86803240 @default.
• W2950685841 hasConceptScore W2950685841C104317684 @default.
• W2950685841 hasConceptScore W2950685841C119056186 @default.
• W2950685841 hasConceptScore W2950685841C121608353 @default.
• W2950685841 hasConceptScore W2950685841C126322002 @default.
• W2950685841 hasConceptScore W2950685841C127716648 @default.
• W2950685841 hasConceptScore W2950685841C143998085 @default.
• W2950685841 hasConceptScore W2950685841C145059251 @default.
• W2950685841 hasConceptScore W2950685841C1491633281 @default.
• W2950685841 hasConceptScore W2950685841C190283241 @default.

• next