Matches in SemOpenAlex for { <https://semopenalex.org/work/W2146295064> ?p ?o ?g. }
- W2146295064 endingPage "63" @default.
- W2146295064 startingPage "57" @default.
- W2146295064 abstract "Interferon (IFN)‐α is one of the most commonly used agents in immunotherapy for patients with advanced stage renal cell carcinoma. However, because of the drug resistance to IFN‐α, its benefits are limited. In this study, we examined whether repression of suppressor of cytokine signaling (SOCS) proteins, which are involved in the IFN‐induced signaling pathway, can overcome the IFN resistance of renal cell carcinoma. The effect of IFN‐α on SOCS3 expression and cell proliferation was examined using IFN‐resistant 786‐O and IFN‐sensitive ACHN cell lines. The effects of SOCS3‐targeted siRNA on 786‐O xenografts were determined by SOCS3 expression, morphological observation, and tumor volume. The SOCS3 mRNA expression level was significantly increased by IFN‐α stimulation in 786‐O, but not in ACHN cells. The overexpression of SOCS3 by gene transfection in ACHN cells significantly inhibited the growth‐inhibitory effect of IFN‐α. Suppression of SOCS3 expression in 786‐O cells by siRNA activated the IFN signaling pathway through signal transducer and activator of transcription 1 phosphorylation and recovered sensitivity to IFN‐α. An in vivo study indicated that co‐administration of SOCS3‐targeted siRNA promoted IFN‐α‐induced cell death and growth suppression in 786‐O cell xenograft in nude mice. Morphological observation of the tumors revealed the inhibition of SOCS3‐induced apoptosis, invasion of inflammatory cells and fibrosis. SOCS3 could be a key component in the resistance to IFN treatment of renal cell carcinoma. Silencing SOCS3 gene expression could be an effective strategy to enhance the antitumor effect of IFN in human renal cell carcinoma cells. ( Cancer Sci 2011; 102: 57–63)" @default.
- W2146295064 created "2016-06-24" @default.
- W2146295064 creator A5001834452 @default.
- W2146295064 creator A5007875223 @default.
- W2146295064 creator A5033408219 @default.
- W2146295064 creator A5041264578 @default.
- W2146295064 creator A5044035162 @default.
- W2146295064 creator A5052084624 @default.
- W2146295064 creator A5062822226 @default.
- W2146295064 creator A5076149190 @default.
- W2146295064 creator A5078409676 @default.
- W2146295064 creator A5081989746 @default.
- W2146295064 creator A5089630337 @default.
- W2146295064 date "2010-11-05" @default.
- W2146295064 modified "2023-10-18" @default.
- W2146295064 title "Suppression of SOCS3 increases susceptibility of renal cell carcinoma to interferon-α" @default.
- W2146295064 cites W1916777958 @default.
- W2146295064 cites W1965464733 @default.
- W2146295064 cites W1976210019 @default.
- W2146295064 cites W1979328748 @default.
- W2146295064 cites W1981745443 @default.
- W2146295064 cites W2001158436 @default.
- W2146295064 cites W2006428522 @default.
- W2146295064 cites W2016757878 @default.
- W2146295064 cites W2019355116 @default.
- W2146295064 cites W2025522989 @default.
- W2146295064 cites W2041881143 @default.
- W2146295064 cites W2045459295 @default.
- W2146295064 cites W2048767389 @default.
- W2146295064 cites W2055446333 @default.
- W2146295064 cites W2060402899 @default.
- W2146295064 cites W2090002359 @default.
- W2146295064 cites W2093442991 @default.
- W2146295064 cites W2100669312 @default.
- W2146295064 cites W2127328515 @default.
- W2146295064 cites W2129205448 @default.
- W2146295064 cites W2138178697 @default.
- W2146295064 cites W2149456801 @default.
- W2146295064 cites W2152152351 @default.
- W2146295064 cites W2153867442 @default.
- W2146295064 cites W2314590426 @default.
- W2146295064 cites W2542515380 @default.
- W2146295064 doi "https://doi.org/10.1111/j.1349-7006.2010.01751.x" @default.
- W2146295064 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21054677" @default.
- W2146295064 hasPublicationYear "2010" @default.
- W2146295064 type Work @default.
- W2146295064 sameAs 2146295064 @default.
- W2146295064 citedByCount "39" @default.
- W2146295064 countsByYear W21462950642012 @default.
- W2146295064 countsByYear W21462950642013 @default.
- W2146295064 countsByYear W21462950642014 @default.
- W2146295064 countsByYear W21462950642015 @default.
- W2146295064 countsByYear W21462950642016 @default.
- W2146295064 countsByYear W21462950642017 @default.
- W2146295064 countsByYear W21462950642018 @default.
- W2146295064 countsByYear W21462950642021 @default.
- W2146295064 countsByYear W21462950642022 @default.
- W2146295064 countsByYear W21462950642023 @default.
- W2146295064 crossrefType "journal-article" @default.
- W2146295064 hasAuthorship W2146295064A5001834452 @default.
- W2146295064 hasAuthorship W2146295064A5007875223 @default.
- W2146295064 hasAuthorship W2146295064A5033408219 @default.
- W2146295064 hasAuthorship W2146295064A5041264578 @default.
- W2146295064 hasAuthorship W2146295064A5044035162 @default.
- W2146295064 hasAuthorship W2146295064A5052084624 @default.
- W2146295064 hasAuthorship W2146295064A5062822226 @default.
- W2146295064 hasAuthorship W2146295064A5076149190 @default.
- W2146295064 hasAuthorship W2146295064A5078409676 @default.
- W2146295064 hasAuthorship W2146295064A5081989746 @default.
- W2146295064 hasAuthorship W2146295064A5089630337 @default.
- W2146295064 hasBestOaLocation W21462950641 @default.
- W2146295064 hasConcept C104317684 @default.
- W2146295064 hasConcept C119056186 @default.
- W2146295064 hasConcept C121608353 @default.
- W2146295064 hasConcept C126042315 @default.
- W2146295064 hasConcept C14077384 @default.
- W2146295064 hasConcept C1491633281 @default.
- W2146295064 hasConcept C171958077 @default.
- W2146295064 hasConcept C179185449 @default.
- W2146295064 hasConcept C203014093 @default.
- W2146295064 hasConcept C2776178377 @default.
- W2146295064 hasConcept C2778690821 @default.
- W2146295064 hasConcept C2778923194 @default.
- W2146295064 hasConcept C502942594 @default.
- W2146295064 hasConcept C54009773 @default.
- W2146295064 hasConcept C54355233 @default.
- W2146295064 hasConcept C55493867 @default.
- W2146295064 hasConcept C62112901 @default.
- W2146295064 hasConcept C62478195 @default.
- W2146295064 hasConcept C81885089 @default.
- W2146295064 hasConcept C86803240 @default.
- W2146295064 hasConcept C95444343 @default.
- W2146295064 hasConceptScore W2146295064C104317684 @default.
- W2146295064 hasConceptScore W2146295064C119056186 @default.
- W2146295064 hasConceptScore W2146295064C121608353 @default.
- W2146295064 hasConceptScore W2146295064C126042315 @default.
- W2146295064 hasConceptScore W2146295064C14077384 @default.
- W2146295064 hasConceptScore W2146295064C1491633281 @default.