FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2910144242> ?p ?o ?g. }

• W2910144242 endingPage "88" @default.
• W2910144242 startingPage "73" @default.
• W2910144242 abstract "Leptin, a hormone primarily derived from adipose tissue, is known to induce tumor growth, but its underlying mechanisms of action are not clearly understood. Inflammasomes, acting as signaling platforms for controlling inflammatory responses, modulate tumor growth in a complicated manner. In this study, we investigated the role of inflammasomes in leptin-induced growth of breast cancer cells. Herein, we showed that leptin activated NLRP3 inflammasomes in MCF-7 breast cancer cells, as determined by activation of caspase-1, maturation of interleukin-1β, and increased expression of the inflammasome components, including NLRP3 and ASC. Interestingly, inhibition of the inflammasome by treatment with a pharmacological inhibitor of caspase-1 or gene silencing of NLRP3 prevented leptin-induced increase in cell viability. Moreover, suppression of apoptosis and cell cycle promotion by leptin were also significantly abolished by gene silencing of NLRP3, clearly indicating a crucial role of NLRP3 inflammasomes in leptin-induced breast cancer growth. In addition, inhibition of estrogen receptor signaling or ROS production markedly blocked leptin-induced activation of NLRP3 inflammasomes, suggesting that estrogen receptor signaling and ROS production mediate inflammasomes activation by leptin. The stimulatory effect of leptin on inflammasomes activation was also observed in MCF-7 tumor xenograft model. Furthermore, the critical roles of inflammasomes activation in leptin-induced tumor growth, suppression of apoptotic gene expression, and induction of the genes stimulating cell cycle were confirmed in a tumor xenograft model. Taken together, these results demonstrate that inflammasomes activation plays a pivotal role in leptin-induced growth of breast cancer cells via modulation of both apoptosis and cell cycle." @default.
• W2910144242 created "2019-01-25" @default.
• W2910144242 creator A5005487766 @default.
• W2910144242 creator A5009209658 @default.
• W2910144242 creator A5016210163 @default.
• W2910144242 creator A5032632529 @default.
• W2910144242 creator A5034268961 @default.
• W2910144242 date "2019-03-01" @default.
• W2910144242 modified "2023-10-16" @default.
• W2910144242 title "Growth of breast cancer cells by leptin is mediated via activation of the inflammasome: Critical roles of estrogen receptor signaling and reactive oxygen species production" @default.
• W2910144242 cites W1520447517 @default.
• W2910144242 cites W1561041814 @default.
• W2910144242 cites W1571499367 @default.
• W2910144242 cites W1604179718 @default.
• W2910144242 cites W1820249097 @default.
• W2910144242 cites W1953948364 @default.
• W2910144242 cites W1954263225 @default.
• W2910144242 cites W1970404468 @default.
• W2910144242 cites W1978468923 @default.
• W2910144242 cites W1986826247 @default.
• W2910144242 cites W1992921465 @default.
• W2910144242 cites W1994561845 @default.
• W2910144242 cites W1994620161 @default.
• W2910144242 cites W1996713062 @default.
• W2910144242 cites W2001380540 @default.
• W2910144242 cites W2011540227 @default.
• W2910144242 cites W2014229457 @default.
• W2910144242 cites W2021857124 @default.
• W2910144242 cites W2029398685 @default.
• W2910144242 cites W2034418213 @default.
• W2910144242 cites W2034773448 @default.
• W2910144242 cites W2052857449 @default.
• W2910144242 cites W2056814151 @default.
• W2910144242 cites W2058590329 @default.
• W2910144242 cites W2064741210 @default.
• W2910144242 cites W2066327704 @default.
• W2910144242 cites W2072914828 @default.
• W2910144242 cites W2084139121 @default.
• W2910144242 cites W2102144390 @default.
• W2910144242 cites W2105256361 @default.
• W2910144242 cites W2118403357 @default.
• W2910144242 cites W2118983602 @default.
• W2910144242 cites W2125382661 @default.
• W2910144242 cites W2135547617 @default.
• W2910144242 cites W2136159290 @default.
• W2910144242 cites W2138791600 @default.
• W2910144242 cites W2140698589 @default.
• W2910144242 cites W2149766325 @default.
• W2910144242 cites W2166209782 @default.
• W2910144242 cites W2167877755 @default.
• W2910144242 cites W2171325859 @default.
• W2910144242 cites W2239996937 @default.
• W2910144242 cites W2265261098 @default.
• W2910144242 cites W2508082015 @default.
• W2910144242 cites W2514420344 @default.
• W2910144242 cites W2529393815 @default.
• W2910144242 cites W2544622388 @default.
• W2910144242 cites W2575182211 @default.
• W2910144242 cites W2600996894 @default.
• W2910144242 cites W2607525892 @default.
• W2910144242 cites W2612043088 @default.
• W2910144242 cites W2622213084 @default.
• W2910144242 cites W2626641390 @default.
• W2910144242 cites W2757522502 @default.
• W2910144242 cites W2766874785 @default.
• W2910144242 cites W2769658100 @default.
• W2910144242 cites W2781525129 @default.
• W2910144242 cites W2803644447 @default.
• W2910144242 cites W2803685835 @default.
• W2910144242 cites W2865060325 @default.
• W2910144242 cites W2884226389 @default.
• W2910144242 cites W2894103177 @default.
• W2910144242 cites W415226552 @default.
• W2910144242 cites W4211217520 @default.
• W2910144242 doi "https://doi.org/10.1016/j.bcp.2019.01.006" @default.
• W2910144242 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30633869" @default.
• W2910144242 hasPublicationYear "2019" @default.
• W2910144242 type Work @default.
• W2910144242 sameAs 2910144242 @default.
• W2910144242 citedByCount "47" @default.
• W2910144242 countsByYear W29101442422019 @default.
• W2910144242 countsByYear W29101442422020 @default.
• W2910144242 countsByYear W29101442422021 @default.
• W2910144242 countsByYear W29101442422022 @default.
• W2910144242 countsByYear W29101442422023 @default.
• W2910144242 crossrefType "journal-article" @default.
• W2910144242 hasAuthorship W2910144242A5005487766 @default.
• W2910144242 hasAuthorship W2910144242A5009209658 @default.
• W2910144242 hasAuthorship W2910144242A5016210163 @default.
• W2910144242 hasAuthorship W2910144242A5032632529 @default.
• W2910144242 hasAuthorship W2910144242A5034268961 @default.
• W2910144242 hasConcept C104317684 @default.
• W2910144242 hasConcept C119056186 @default.
• W2910144242 hasConcept C121608353 @default.
• W2910144242 hasConcept C126322002 @default.
• W2910144242 hasConcept C134018914 @default.
• W2910144242 hasConcept C170493617 @default.
• W2910144242 hasConcept C185592680 @default.

• next