FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2899164585> ?p ?o ?g. }

• W2899164585 endingPage "5112" @default.
• W2899164585 startingPage "5101" @default.
• W2899164585 abstract "Downregulation of PIM1 regulates glycolysis and suppresses tumor progression in gallbladder cancer Chen Xue,1,2,* Yuting He,1,2,* Qiuyue Hu,1,2 Yan Yu,1,2 Xiaolong Chen,1,2 Jianan Chen,1,2 Fang Ren,2 Juan Li,1,2 Zhigang Ren,1,2 Guangying Cui,1,2 Ranran Sun1–3 1Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; 2Key Laboratory of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China; 3National Engineering Laboratory for Internet Medical Systems and Applications, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China *These authors contributed equally to this work Background: PIM1, a serine/threonine kinase, plays an essential role in tumorigenesis of multiple types of tumors. However, the expression pattern and functions of PIM1 in gallbladder cancer (GBC) remain largely unknown. Materials and methods: Immunohistochemistry, quantitative real-time PCR, and western blot analysis were performed to measure the expression of PIM1. Tissue microarray analysis was used to confirm the relationship between PIM1 expression and clinical outcomes of GBC patients. Finally, in vivo and in vitro functional studies were performed to detect the inhibition of PIM1 by RNAi or specific inhibitor in GBC cells. Results: We observed that PIM1 was dramatically overexpressed in GBC tissues, and its expression levels were positively related with clinical malignancies and a poor prognosis. Inhibition of PIM1 via RNAi or enzyme-specific inhibitor could suppress GBC cell proliferation, migration, and invasion both in vitro and vivo. Additionally, flow cytometry assays and cell cycle assays indicated that PIM1 inhibition promoted cell apoptosis and induced cell cycle arrest. Remarkably, inhibition of PIM1 could drive a metabolic shift from aerobic glycolysis to oxidative phosphorylation. We found that inhibition of PIM1 mechanistically reduced glucose consumption by regulating key molecules in aerobic glycolysis. Conclusion: PIM1 may serve as an oncogene in GBC and be involved in the regulation of glycolysis. PIM1 is a promising therapeutic target for the treatment of human GBC. Keywords: PIM1, gallbladder cancer, aerobic glycolysis, tumor progression" @default.
• W2899164585 created "2018-11-09" @default.
• W2899164585 creator A5003281764 @default.
• W2899164585 creator A5011631723 @default.
• W2899164585 creator A5017119373 @default.
• W2899164585 creator A5030303113 @default.
• W2899164585 creator A5033031458 @default.
• W2899164585 creator A5049872422 @default.
• W2899164585 creator A5053415959 @default.
• W2899164585 creator A5064711465 @default.
• W2899164585 creator A5065141144 @default.
• W2899164585 creator A5073364442 @default.
• W2899164585 creator A5085570062 @default.
• W2899164585 date "2018-10-01" @default.
• W2899164585 modified "2023-09-24" @default.
• W2899164585 title "Downregulation of PIM1 regulates glycolysis and suppresses tumor progression in gallbladder cancer" @default.
• W2899164585 cites W1500418465 @default.
• W2899164585 cites W1665091651 @default.
• W2899164585 cites W2035132997 @default.
• W2899164585 cites W2052944775 @default.
• W2899164585 cites W2062393446 @default.
• W2899164585 cites W2065588058 @default.
• W2899164585 cites W2087350855 @default.
• W2899164585 cites W2099825600 @default.
• W2899164585 cites W2102877084 @default.
• W2899164585 cites W2103935957 @default.
• W2899164585 cites W2132501730 @default.
• W2899164585 cites W2149266461 @default.
• W2899164585 cites W2160588684 @default.
• W2899164585 cites W2171218023 @default.
• W2899164585 cites W2297905586 @default.
• W2899164585 cites W2300979116 @default.
• W2899164585 cites W2403268374 @default.
• W2899164585 cites W2534173999 @default.
• W2899164585 cites W2536094308 @default.
• W2899164585 cites W2619021353 @default.
• W2899164585 cites W2735874885 @default.
• W2899164585 cites W2737670341 @default.
• W2899164585 cites W2754515846 @default.
• W2899164585 cites W2790323243 @default.
• W2899164585 cites W2790518568 @default.
• W2899164585 cites W2791680476 @default.
• W2899164585 cites W2792724222 @default.
• W2899164585 cites W2794640770 @default.
• W2899164585 cites W2883009647 @default.
• W2899164585 cites W2886379647 @default.
• W2899164585 doi "https://doi.org/10.2147/cmar.s184381" @default.
• W2899164585 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6215917" @default.
• W2899164585 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30464610" @default.
• W2899164585 hasPublicationYear "2018" @default.
• W2899164585 type Work @default.
• W2899164585 sameAs 2899164585 @default.
• W2899164585 citedByCount "18" @default.
• W2899164585 countsByYear W28991645852019 @default.
• W2899164585 countsByYear W28991645852020 @default.
• W2899164585 countsByYear W28991645852021 @default.
• W2899164585 countsByYear W28991645852022 @default.
• W2899164585 countsByYear W28991645852023 @default.
• W2899164585 crossrefType "journal-article" @default.
• W2899164585 hasAuthorship W2899164585A5003281764 @default.
• W2899164585 hasAuthorship W2899164585A5011631723 @default.
• W2899164585 hasAuthorship W2899164585A5017119373 @default.
• W2899164585 hasAuthorship W2899164585A5030303113 @default.
• W2899164585 hasAuthorship W2899164585A5033031458 @default.
• W2899164585 hasAuthorship W2899164585A5049872422 @default.
• W2899164585 hasAuthorship W2899164585A5053415959 @default.
• W2899164585 hasAuthorship W2899164585A5064711465 @default.
• W2899164585 hasAuthorship W2899164585A5065141144 @default.
• W2899164585 hasAuthorship W2899164585A5073364442 @default.
• W2899164585 hasAuthorship W2899164585A5085570062 @default.
• W2899164585 hasBestOaLocation W28991645851 @default.
• W2899164585 hasConcept C104317684 @default.
• W2899164585 hasConcept C11960822 @default.
• W2899164585 hasConcept C121608353 @default.
• W2899164585 hasConcept C126322002 @default.
• W2899164585 hasConcept C127561419 @default.
• W2899164585 hasConcept C150903083 @default.
• W2899164585 hasConcept C207001950 @default.
• W2899164585 hasConcept C2776414213 @default.
• W2899164585 hasConcept C502942594 @default.
• W2899164585 hasConcept C55493867 @default.
• W2899164585 hasConcept C555283112 @default.
• W2899164585 hasConcept C71924100 @default.
• W2899164585 hasConcept C86803240 @default.
• W2899164585 hasConcept C95444343 @default.
• W2899164585 hasConcept C98175054 @default.
• W2899164585 hasConceptScore W2899164585C104317684 @default.
• W2899164585 hasConceptScore W2899164585C11960822 @default.
• W2899164585 hasConceptScore W2899164585C121608353 @default.
• W2899164585 hasConceptScore W2899164585C126322002 @default.
• W2899164585 hasConceptScore W2899164585C127561419 @default.
• W2899164585 hasConceptScore W2899164585C150903083 @default.
• W2899164585 hasConceptScore W2899164585C207001950 @default.
• W2899164585 hasConceptScore W2899164585C2776414213 @default.
• W2899164585 hasConceptScore W2899164585C502942594 @default.
• W2899164585 hasConceptScore W2899164585C55493867 @default.
• W2899164585 hasConceptScore W2899164585C555283112 @default.
• W2899164585 hasConceptScore W2899164585C71924100 @default.

• next