Matches in SemOpenAlex for { <https://semopenalex.org/work/W2808206919> ?p ?o ?g. }
- W2808206919 abstract "Hepatocellular carcinoma (HCC) is the sixth most common cancer and the second leading cause of cancer-related deaths worldwide. Despite new technologies in diagnosis and treatment, the incidence and mortality of HCC continue rising. And its pathogenesis is still unclear. As a highly conserved protein of the Golgi apparatus, Golgi phosphoprotein 3 (GOLPH3) has been shown to be involved in tumorigenesis of HCC. This study aimed to explore the exact oncogenic mechanism of GOLPH3 and provide a novel diagnose biomarker and therapeutic strategy for patients with HCC. Firstly, the expression of GOLPH3 was detected in the HCC tissue specimens and HCC cell lines. Secondly, RNA interference was used for GOLPH3 gene inhibition. Thirdly, cell proliferation was analyzed by MTT; cell apoptosis was analyzed by Annexin-V/PI staining, Hoechst 33,342 staining and caspase 3/7 activity assay. Fourthly, xenograft tumor model was used to study the function of GOLPH3 in tumor growth in vivo. Finally, western blotting and immunohistochemistry were used to investigate the role of GOLHP3 in the mTOR signaling pathway. Data showed that the mRNA and protein expression of GOLPH3 were up-regulated in HCC tumor tissue and cell lines compared with those of control (P < 0.05). Correlation analyses showed that GOLPH3 expression was positively correlated with serum alpha-fetoprotein level (AFP, P = 0.006). Knockdown GOLPH3 expression inhibited proliferation and promoted apoptosis in HCC cell lines. What’s more, knockdown GOLPH3 expression led to tumor growth restriction in xenograft tumor model. The expression of phosphorylated mTOR, AKT and S6 K1 were significantly higher in HCC tumor tissue and cell lines compared with those in normal liver tissues (p < 0.05). While the phosphorylated mTOR, AKT and S6 K1 were much lower when diminished GOLPH3 expression in HCC cell lines both in vitro and in vivo. The current study suggests that GOLPH3 contributes to the tumorigenesis of HCC by activating mTOR signaling pathway. GOLPH3 is a promising diagnose biomarker and therapeutic target for HCC. Our study may provide a scientific basis for developing effective approaches to treat the HCC patients with GOLPH3 overexpression." @default.
- W2808206919 created "2018-06-21" @default.
- W2808206919 creator A5011101778 @default.
- W2808206919 creator A5023564935 @default.
- W2808206919 creator A5038914624 @default.
- W2808206919 creator A5043398854 @default.
- W2808206919 creator A5058759390 @default.
- W2808206919 creator A5060667885 @default.
- W2808206919 creator A5066364199 @default.
- W2808206919 creator A5077343172 @default.
- W2808206919 creator A5077622519 @default.
- W2808206919 creator A5087983120 @default.
- W2808206919 date "2018-06-18" @default.
- W2808206919 modified "2023-10-18" @default.
- W2808206919 title "Golgi phosphoprotein 3 (GOLPH3) promotes hepatocellular carcinoma progression by activating mTOR signaling pathway" @default.
- W2808206919 cites W1668086213 @default.
- W2808206919 cites W1757407923 @default.
- W2808206919 cites W1965766554 @default.
- W2808206919 cites W1974942240 @default.
- W2808206919 cites W1984621921 @default.
- W2808206919 cites W1984736455 @default.
- W2808206919 cites W1997530857 @default.
- W2808206919 cites W1999056466 @default.
- W2808206919 cites W1999365630 @default.
- W2808206919 cites W2000971652 @default.
- W2808206919 cites W2012675034 @default.
- W2808206919 cites W2022633334 @default.
- W2808206919 cites W2023012828 @default.
- W2808206919 cites W2035016947 @default.
- W2808206919 cites W2036691369 @default.
- W2808206919 cites W2048391838 @default.
- W2808206919 cites W2050880187 @default.
- W2808206919 cites W2053306127 @default.
- W2808206919 cites W2053643795 @default.
- W2808206919 cites W2063986127 @default.
- W2808206919 cites W2073547855 @default.
- W2808206919 cites W2080100938 @default.
- W2808206919 cites W2082341788 @default.
- W2808206919 cites W2084119969 @default.
- W2808206919 cites W2084849608 @default.
- W2808206919 cites W2095537445 @default.
- W2808206919 cites W2101546320 @default.
- W2808206919 cites W2109490882 @default.
- W2808206919 cites W2119071017 @default.
- W2808206919 cites W2123359660 @default.
- W2808206919 cites W2137794715 @default.
- W2808206919 cites W2143254803 @default.
- W2808206919 cites W2148163986 @default.
- W2808206919 cites W2161489444 @default.
- W2808206919 cites W2272984102 @default.
- W2808206919 cites W2284758093 @default.
- W2808206919 cites W2346764222 @default.
- W2808206919 cites W2405603149 @default.
- W2808206919 cites W2526391756 @default.
- W2808206919 cites W2754171162 @default.
- W2808206919 cites W3141418844 @default.
- W2808206919 cites W4238567307 @default.
- W2808206919 doi "https://doi.org/10.1186/s12885-018-4458-7" @default.
- W2808206919 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6006993" @default.
- W2808206919 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29914442" @default.
- W2808206919 hasPublicationYear "2018" @default.
- W2808206919 type Work @default.
- W2808206919 sameAs 2808206919 @default.
- W2808206919 citedByCount "24" @default.
- W2808206919 countsByYear W28082069192019 @default.
- W2808206919 countsByYear W28082069192020 @default.
- W2808206919 countsByYear W28082069192021 @default.
- W2808206919 countsByYear W28082069192022 @default.
- W2808206919 countsByYear W28082069192023 @default.
- W2808206919 crossrefType "journal-article" @default.
- W2808206919 hasAuthorship W2808206919A5011101778 @default.
- W2808206919 hasAuthorship W2808206919A5023564935 @default.
- W2808206919 hasAuthorship W2808206919A5038914624 @default.
- W2808206919 hasAuthorship W2808206919A5043398854 @default.
- W2808206919 hasAuthorship W2808206919A5058759390 @default.
- W2808206919 hasAuthorship W2808206919A5060667885 @default.
- W2808206919 hasAuthorship W2808206919A5066364199 @default.
- W2808206919 hasAuthorship W2808206919A5077343172 @default.
- W2808206919 hasAuthorship W2808206919A5077622519 @default.
- W2808206919 hasAuthorship W2808206919A5087983120 @default.
- W2808206919 hasBestOaLocation W28082069191 @default.
- W2808206919 hasConcept C121608353 @default.
- W2808206919 hasConcept C173396325 @default.
- W2808206919 hasConcept C190283241 @default.
- W2808206919 hasConcept C502942594 @default.
- W2808206919 hasConcept C54355233 @default.
- W2808206919 hasConcept C55493867 @default.
- W2808206919 hasConcept C555283112 @default.
- W2808206919 hasConcept C62112901 @default.
- W2808206919 hasConcept C62478195 @default.
- W2808206919 hasConcept C75217442 @default.
- W2808206919 hasConcept C86554907 @default.
- W2808206919 hasConcept C86803240 @default.
- W2808206919 hasConcept C95444343 @default.
- W2808206919 hasConceptScore W2808206919C121608353 @default.
- W2808206919 hasConceptScore W2808206919C173396325 @default.
- W2808206919 hasConceptScore W2808206919C190283241 @default.
- W2808206919 hasConceptScore W2808206919C502942594 @default.
- W2808206919 hasConceptScore W2808206919C54355233 @default.
- W2808206919 hasConceptScore W2808206919C55493867 @default.