Matches in SemOpenAlex for { <https://semopenalex.org/work/W2100060697> ?p ?o ?g. }
- W2100060697 endingPage "2134" @default.
- W2100060697 startingPage "2125" @default.
- W2100060697 abstract "HOXA1 overexpression is sufficient for malignant transformation of nontumorigenic epithelial cells. It is known that HOXA1, which was upregulated in squamous cell carcinomas, affects both cell growth and death. The forced expression of HOXA1 in human breast cancer cells results in increased cell growth activity. However, it has not been reported in hepatocellular carcinoma (HCC). In this study, we used immunohistochemistry to compare HOXA1 protein expression in HCC and normal liver tissues and further analyzed HOXA1 protein expression in 156 clinicopathologically characterized HCC cases. We stably knocked down the endogenous expression level of HOXA1 in HepG2 cells with specific shRNA-expressing lentiviral vector. Following the successful establishment of stable cells, we examined in vitro cell growth by the MTT assay, anchorage-independent growth through a soft agar colony formation assay and cell migration/invasion by transwell and Boyden chamber assay. In addition, we also investigated in vivo tumor growth by xenograft transplantation of HepG2 cells into nude mice. Our results showed that the protein expression level of HOXA1 was markedly higher in HCC tissues than that in normal liver tissue (P = 0.019). In addition, a high expression level of HOXA1 protein was positively correlated with the T classification (P < 0.001), the N classification (P < 0.001), distant metastasis (P = 0.004), and the clinical stage (P < 0.001) of HCC patients. Patients with higher HOXA1 expression showed a significantly shorter overall survival time compared with patients with low HOXA1 expression. Multivariate analysis suggested that HOXA1 expression might be an independent prognostic indicator (P < 0.001) for the survival of patients with HCC. HOXA1-specific shRNA (shHOXA1) successfully knocked down HOXA1 endogenous expression in HepG2 cells. Compared to the parental and control shRNA-transfected (shCtrl) HepG2 cells, the shHOXA1 cells exhibited significantly reduced in vitro cell growth, anchorage-independent growth, and cell migration and invasion (P < 0.05). In vivo, the xenograft transplants from shHOXA1 cells gave rise to much smaller tumors compared with those from shCtrl cells. Collectively, high HOXA1 expression is associated with poor overall survival in patients with HCC. The downregulation of HOXA1 inhibits growth, anchorage-independent growth, and migration and invasion of HepG2 cells." @default.
- W2100060697 created "2016-06-24" @default.
- W2100060697 creator A5018071594 @default.
- W2100060697 creator A5024811010 @default.
- W2100060697 creator A5026047112 @default.
- W2100060697 creator A5042050423 @default.
- W2100060697 creator A5060208750 @default.
- W2100060697 creator A5066497348 @default.
- W2100060697 date "2012-08-04" @default.
- W2100060697 modified "2023-09-28" @default.
- W2100060697 title "Overexpression of HOXA1 correlates with poor prognosis in patients with hepatocellular carcinoma" @default.
- W2100060697 cites W1972249702 @default.
- W2100060697 cites W1983218872 @default.
- W2100060697 cites W1997105018 @default.
- W2100060697 cites W1997632855 @default.
- W2100060697 cites W2009988711 @default.
- W2100060697 cites W2011701848 @default.
- W2100060697 cites W2037700462 @default.
- W2100060697 cites W2047790795 @default.
- W2100060697 cites W2056746886 @default.
- W2100060697 cites W2058845682 @default.
- W2100060697 cites W2066171378 @default.
- W2100060697 cites W2076229847 @default.
- W2100060697 cites W2088629624 @default.
- W2100060697 cites W2097934124 @default.
- W2100060697 cites W2101302062 @default.
- W2100060697 cites W2118434971 @default.
- W2100060697 cites W2134303676 @default.
- W2100060697 cites W2146122330 @default.
- W2100060697 cites W2154576630 @default.
- W2100060697 cites W2158117506 @default.
- W2100060697 cites W58991659 @default.
- W2100060697 doi "https://doi.org/10.1007/s13277-012-0472-6" @default.
- W2100060697 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22864671" @default.
- W2100060697 hasPublicationYear "2012" @default.
- W2100060697 type Work @default.
- W2100060697 sameAs 2100060697 @default.
- W2100060697 citedByCount "41" @default.
- W2100060697 countsByYear W21000606972013 @default.
- W2100060697 countsByYear W21000606972014 @default.
- W2100060697 countsByYear W21000606972015 @default.
- W2100060697 countsByYear W21000606972016 @default.
- W2100060697 countsByYear W21000606972017 @default.
- W2100060697 countsByYear W21000606972018 @default.
- W2100060697 countsByYear W21000606972019 @default.
- W2100060697 countsByYear W21000606972020 @default.
- W2100060697 countsByYear W21000606972021 @default.
- W2100060697 countsByYear W21000606972022 @default.
- W2100060697 countsByYear W21000606972023 @default.
- W2100060697 crossrefType "journal-article" @default.
- W2100060697 hasAuthorship W2100060697A5018071594 @default.
- W2100060697 hasAuthorship W2100060697A5024811010 @default.
- W2100060697 hasAuthorship W2100060697A5026047112 @default.
- W2100060697 hasAuthorship W2100060697A5042050423 @default.
- W2100060697 hasAuthorship W2100060697A5060208750 @default.
- W2100060697 hasAuthorship W2100060697A5066497348 @default.
- W2100060697 hasConcept C104317684 @default.
- W2100060697 hasConcept C121608353 @default.
- W2100060697 hasConcept C126322002 @default.
- W2100060697 hasConcept C127561419 @default.
- W2100060697 hasConcept C142724271 @default.
- W2100060697 hasConcept C1491633281 @default.
- W2100060697 hasConcept C203014093 @default.
- W2100060697 hasConcept C204232928 @default.
- W2100060697 hasConcept C2778019345 @default.
- W2100060697 hasConcept C2911091166 @default.
- W2100060697 hasConcept C502942594 @default.
- W2100060697 hasConcept C54355233 @default.
- W2100060697 hasConcept C55493867 @default.
- W2100060697 hasConcept C62112901 @default.
- W2100060697 hasConcept C71924100 @default.
- W2100060697 hasConcept C81885089 @default.
- W2100060697 hasConcept C86803240 @default.
- W2100060697 hasConceptScore W2100060697C104317684 @default.
- W2100060697 hasConceptScore W2100060697C121608353 @default.
- W2100060697 hasConceptScore W2100060697C126322002 @default.
- W2100060697 hasConceptScore W2100060697C127561419 @default.
- W2100060697 hasConceptScore W2100060697C142724271 @default.
- W2100060697 hasConceptScore W2100060697C1491633281 @default.
- W2100060697 hasConceptScore W2100060697C203014093 @default.
- W2100060697 hasConceptScore W2100060697C204232928 @default.
- W2100060697 hasConceptScore W2100060697C2778019345 @default.
- W2100060697 hasConceptScore W2100060697C2911091166 @default.
- W2100060697 hasConceptScore W2100060697C502942594 @default.
- W2100060697 hasConceptScore W2100060697C54355233 @default.
- W2100060697 hasConceptScore W2100060697C55493867 @default.
- W2100060697 hasConceptScore W2100060697C62112901 @default.
- W2100060697 hasConceptScore W2100060697C71924100 @default.
- W2100060697 hasConceptScore W2100060697C81885089 @default.
- W2100060697 hasConceptScore W2100060697C86803240 @default.
- W2100060697 hasIssue "6" @default.
- W2100060697 hasLocation W21000606971 @default.
- W2100060697 hasLocation W21000606972 @default.
- W2100060697 hasOpenAccess W2100060697 @default.
- W2100060697 hasPrimaryLocation W21000606971 @default.
- W2100060697 hasRelatedWork W1983015622 @default.
- W2100060697 hasRelatedWork W2028625067 @default.
- W2100060697 hasRelatedWork W2285430460 @default.