FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2887672801> ?p ?o ?g. }

• W2887672801 endingPage "2421" @default.
• W2887672801 startingPage "2413" @default.
• W2887672801 abstract "Sinomenine inhibits the growth of melanoma by enhancement of autophagy via PI3K/AKT/mTOR inhibition Zheng Sun,1 Lingling Zheng,1 Xujun Liu,2 Wenlong Xing,3 Xinhai Liu4 1Department of Dermatology and Venereology, Beijing Luhe Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People’s Republic of China; 3Department of Cardiovasology, Beijing Chinese Medicine Hospital, Capital Medical University, Beijing, People’s Republic of China; 4Department of Plastic Surgery, Beijing Luhe Hospital, Capital Medical University, Beijing, People’s Republic of China Background: Melanoma is a common skin tumor in adults with high metastasis and mortality rates. Thus, finding a better effective approach to treat melanoma has become very urgent. Sinomenine (SIN), the major active compound of Sinomenium acutum, has shown antitumorigenic activities in certain cancers. However, its role in melanoma remains unclear. Purpose: This study aimed to explore the effects of SIN on melanoma in vitro and in vivo, in addition to exploring the underlying mechanism. Methods: Mouse melanoma cell B16-F10 treated by SIN was analyzed by CCK8 assay and flow cytometry. Melanoma xenograft model was then established by subcutaneously injection with B16-F10 cells. Tumor growth was measured by immunohistochemistry. To further investigate the relative mechanism, the autophagy and PI3K/Akt/mTOR pathway were examined by immunofluorescence and Western blot. Results: Our results revealed that SIN dose dependently inhibited the proliferation of B16-F10 cells in vitro and attenuated melanoma growth in vivo. In addition, SIN treatment promoted the apoptosis of B16-F10 cells in a dose-dependent manner, as demonstrated by the increase in apoptotic cells, Bax/Bcl-2 ratio, and caspase-3 activity. Moreover, preconditioning with SIN dramatically enhanced autophagy activity by increasing Beclin-1 and LC3II/LC3I expression, in addition to decreasing p62 expression and augmenting the number of LC3 puncta, in B16-F10 cells. More importantly, autophagy inhibitor chloroquine partly abolished SIN’s effects on cell growth and apoptosis. Furthermore, our results showed that SIN-triggered activation of autophagy was mediated by PI3K/Akt/mTOR signaling pathway. Conclusion: Our study has identified a novel function of SIN and provided a molecular basis for potential applications of SIN in the treatment of melanoma and other cancers. Keywords: sinomenine, melanoma, autophagy, PI3K/Akt/mTOR" @default.
• W2887672801 created "2018-08-22" @default.
• W2887672801 creator A5007736125 @default.
• W2887672801 creator A5037977519 @default.
• W2887672801 creator A5056694404 @default.
• W2887672801 creator A5059916828 @default.
• W2887672801 creator A5067506039 @default.
• W2887672801 date "2018-08-01" @default.
• W2887672801 modified "2023-10-15" @default.
• W2887672801 title "Sinomenine inhibits the growth of melanoma by enhancement of autophagy via PI3K/AKT/mTOR inhibition" @default.
• W2887672801 cites W1975962038 @default.
• W2887672801 cites W1987334812 @default.
• W2887672801 cites W1987334928 @default.
• W2887672801 cites W1991692801 @default.
• W2887672801 cites W1996114270 @default.
• W2887672801 cites W1999306559 @default.
• W2887672801 cites W2002636911 @default.
• W2887672801 cites W2003380425 @default.
• W2887672801 cites W2012555541 @default.
• W2887672801 cites W2018799204 @default.
• W2887672801 cites W2035722419 @default.
• W2887672801 cites W2040383220 @default.
• W2887672801 cites W2044638102 @default.
• W2887672801 cites W2059388879 @default.
• W2887672801 cites W2073333066 @default.
• W2887672801 cites W2077195956 @default.
• W2887672801 cites W2078184757 @default.
• W2887672801 cites W2086528604 @default.
• W2887672801 cites W2087607531 @default.
• W2887672801 cites W2089074573 @default.
• W2887672801 cites W2099037538 @default.
• W2887672801 cites W2100403858 @default.
• W2887672801 cites W2105114667 @default.
• W2887672801 cites W2140912399 @default.
• W2887672801 cites W2172338503 @default.
• W2887672801 cites W2400015184 @default.
• W2887672801 cites W2405985041 @default.
• W2887672801 cites W2530326807 @default.
• W2887672801 cites W2556747616 @default.
• W2887672801 cites W2577915723 @default.
• W2887672801 cites W2736629949 @default.
• W2887672801 cites W2768203510 @default.
• W2887672801 cites W2781490082 @default.
• W2887672801 cites W55065340 @default.
• W2887672801 cites W808397578 @default.
• W2887672801 doi "https://doi.org/10.2147/dddt.s155798" @default.
• W2887672801 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6084074" @default.
• W2887672801 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30122899" @default.
• W2887672801 hasPublicationYear "2018" @default.
• W2887672801 type Work @default.
• W2887672801 sameAs 2887672801 @default.
• W2887672801 citedByCount "24" @default.
• W2887672801 countsByYear W28876728012019 @default.
• W2887672801 countsByYear W28876728012020 @default.
• W2887672801 countsByYear W28876728012021 @default.
• W2887672801 countsByYear W28876728012022 @default.
• W2887672801 countsByYear W28876728012023 @default.
• W2887672801 crossrefType "journal-article" @default.
• W2887672801 hasAuthorship W2887672801A5007736125 @default.
• W2887672801 hasAuthorship W2887672801A5037977519 @default.
• W2887672801 hasAuthorship W2887672801A5056694404 @default.
• W2887672801 hasAuthorship W2887672801A5059916828 @default.
• W2887672801 hasAuthorship W2887672801A5067506039 @default.
• W2887672801 hasBestOaLocation W28876728011 @default.
• W2887672801 hasConcept C17744445 @default.
• W2887672801 hasConcept C190283241 @default.
• W2887672801 hasConcept C191935318 @default.
• W2887672801 hasConcept C199539241 @default.
• W2887672801 hasConcept C203014093 @default.
• W2887672801 hasConcept C203522944 @default.
• W2887672801 hasConcept C2777658100 @default.
• W2887672801 hasConcept C2778304055 @default.
• W2887672801 hasConcept C502942594 @default.
• W2887672801 hasConcept C54355233 @default.
• W2887672801 hasConcept C55493867 @default.
• W2887672801 hasConcept C556039675 @default.
• W2887672801 hasConcept C62112901 @default.
• W2887672801 hasConcept C62478195 @default.
• W2887672801 hasConcept C71924100 @default.
• W2887672801 hasConcept C75217442 @default.
• W2887672801 hasConcept C86554907 @default.
• W2887672801 hasConcept C86803240 @default.
• W2887672801 hasConcept C95444343 @default.
• W2887672801 hasConceptScore W2887672801C17744445 @default.
• W2887672801 hasConceptScore W2887672801C190283241 @default.
• W2887672801 hasConceptScore W2887672801C191935318 @default.
• W2887672801 hasConceptScore W2887672801C199539241 @default.
• W2887672801 hasConceptScore W2887672801C203014093 @default.
• W2887672801 hasConceptScore W2887672801C203522944 @default.
• W2887672801 hasConceptScore W2887672801C2777658100 @default.
• W2887672801 hasConceptScore W2887672801C2778304055 @default.
• W2887672801 hasConceptScore W2887672801C502942594 @default.
• W2887672801 hasConceptScore W2887672801C54355233 @default.
• W2887672801 hasConceptScore W2887672801C55493867 @default.
• W2887672801 hasConceptScore W2887672801C556039675 @default.
• W2887672801 hasConceptScore W2887672801C62112901 @default.
• W2887672801 hasConceptScore W2887672801C62478195 @default.
• W2887672801 hasConceptScore W2887672801C71924100 @default.

• next