FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890154310> ?p ?o ?g. }

• W2890154310 endingPage "133" @default.
• W2890154310 startingPage "122" @default.
• W2890154310 abstract "The current obesity pandemic represents a major health burden, given that it predisposes to the development of numerous obesity-associated disorders. The obesity-derived adipokines not only impair systemic insulin action but also increase the incidence of hepatocellular carcinoma (HCC), a highly prevalent cancer with poor prognosis. Thus, worldwide incidences of HCC are expected to further increase, and defining the molecular as well as cellular mechanisms will allow for establishing new potential treatment options. The adipose tissue of obese individuals increases circulating leptin and interleukin-6 (IL-6) levels, which both share similar signaling capacities such as Signal Transducer and Activator of Transcription 3 (STAT3) and Phosphoinositide 3-kinase (PI3K)/Akt activation. While mouse models with deficient IL-6 signaling show an ameliorated but not absent Diethylnitrosamine (DEN)-induced HCC development, the morbid obesity in mice with mutant leptin signaling complicates the dissection of hepatic leptin receptor (LEPR) and IL-6 signaling in HCC development. Here we have investigated the function of compensating hepatic LEPR expression in HCC development of IL-6Rα-deficient mice. We generated and characterized a mouse model of hepatic LEPR deficiency that was intercrossed with IL-6Rα-deficient mice. Cohorts of single and double knockout mice were subjected to the DEN-HCC model to ascertain liver cancer development and characterize metabolic alterations. We demonstrate that both high-fat diet (HFD)-induced obesity and IL-6Rα deficiency induce hepatic Lepr expression. Consistently, double knockout mice show a further reduction in tumor burden in DEN-induced HCC when compared to control and single LepRL−KO/IL-6Rα knock out mice, whereas metabolism remained largely unaltered between the genotypes. Our findings reveal a compensatory role for hepatic LEPR in HCC development of IL-6Rα-deficient mice and suggest hepatocyte-specific leptin signaling as promoter of HCC under obese conditions." @default.
• W2890154310 created "2018-09-27" @default.
• W2890154310 creator A5009505537 @default.
• W2890154310 creator A5025280358 @default.
• W2890154310 creator A5052196227 @default.
• W2890154310 creator A5072937215 @default.
• W2890154310 creator A5088384506 @default.
• W2890154310 creator A5088451932 @default.
• W2890154310 creator A5090554238 @default.
• W2890154310 date "2018-11-01" @default.
• W2890154310 modified "2023-10-15" @default.
• W2890154310 title "Hepatic leptin receptor expression can partially compensate for IL-6Rα deficiency in DEN-induced hepatocellular carcinoma" @default.
• W2890154310 cites W1232974837 @default.
• W2890154310 cites W1506453366 @default.
• W2890154310 cites W1631449371 @default.
• W2890154310 cites W1757407923 @default.
• W2890154310 cites W1953357409 @default.
• W2890154310 cites W1960110193 @default.
• W2890154310 cites W1969674061 @default.
• W2890154310 cites W1978139448 @default.
• W2890154310 cites W1978224578 @default.
• W2890154310 cites W1978281808 @default.
• W2890154310 cites W1980330982 @default.
• W2890154310 cites W1980800789 @default.
• W2890154310 cites W1981401469 @default.
• W2890154310 cites W1983734516 @default.
• W2890154310 cites W1990692512 @default.
• W2890154310 cites W1996713062 @default.
• W2890154310 cites W1998314203 @default.
• W2890154310 cites W2000307707 @default.
• W2890154310 cites W2005176113 @default.
• W2890154310 cites W2005584997 @default.
• W2890154310 cites W2006434448 @default.
• W2890154310 cites W2016129823 @default.
• W2890154310 cites W2016153546 @default.
• W2890154310 cites W2018460745 @default.
• W2890154310 cites W2020114264 @default.
• W2890154310 cites W2022716990 @default.
• W2890154310 cites W2027339934 @default.
• W2890154310 cites W2031650042 @default.
• W2890154310 cites W2039749588 @default.
• W2890154310 cites W2039845199 @default.
• W2890154310 cites W2040901874 @default.
• W2890154310 cites W2043188148 @default.
• W2890154310 cites W2044153433 @default.
• W2890154310 cites W2045934419 @default.
• W2890154310 cites W2046052197 @default.
• W2890154310 cites W2046396043 @default.
• W2890154310 cites W2051192888 @default.
• W2890154310 cites W2052656103 @default.
• W2890154310 cites W2056383195 @default.
• W2890154310 cites W2060313221 @default.
• W2890154310 cites W2060682066 @default.
• W2890154310 cites W2065028165 @default.
• W2890154310 cites W2065825082 @default.
• W2890154310 cites W2068300548 @default.
• W2890154310 cites W2071045528 @default.
• W2890154310 cites W2071589836 @default.
• W2890154310 cites W2076341209 @default.
• W2890154310 cites W2079959936 @default.
• W2890154310 cites W2080998956 @default.
• W2890154310 cites W2087133453 @default.
• W2890154310 cites W2087639358 @default.
• W2890154310 cites W2087962053 @default.
• W2890154310 cites W2088266150 @default.
• W2890154310 cites W2089569798 @default.
• W2890154310 cites W2090699565 @default.
• W2890154310 cites W2093431913 @default.
• W2890154310 cites W2095568085 @default.
• W2890154310 cites W2100386453 @default.
• W2890154310 cites W2100478793 @default.
• W2890154310 cites W2104643975 @default.
• W2890154310 cites W2111796479 @default.
• W2890154310 cites W2112662882 @default.
• W2890154310 cites W2114907597 @default.
• W2890154310 cites W2116662308 @default.
• W2890154310 cites W2118278569 @default.
• W2890154310 cites W2119601529 @default.
• W2890154310 cites W2120970673 @default.
• W2890154310 cites W2122323193 @default.
• W2890154310 cites W2125510262 @default.
• W2890154310 cites W2126184562 @default.
• W2890154310 cites W2129316761 @default.
• W2890154310 cites W2129615992 @default.
• W2890154310 cites W2129785124 @default.
• W2890154310 cites W2136024338 @default.
• W2890154310 cites W2137052325 @default.
• W2890154310 cites W2137257146 @default.
• W2890154310 cites W2141662760 @default.
• W2890154310 cites W2155552970 @default.
• W2890154310 cites W2162797083 @default.
• W2890154310 cites W2163752014 @default.
• W2890154310 cites W2165334726 @default.
• W2890154310 cites W2165778365 @default.
• W2890154310 cites W2165806251 @default.
• W2890154310 cites W2174804804 @default.
• W2890154310 cites W2312252916 @default.
• W2890154310 cites W2339362554 @default.

• next