J
Jin Dai
Researcher at University of Kentucky
Publications - 12
Citations - 585
Jin Dai is an academic researcher from University of Kentucky. The author has contributed to research in topics: Carcinogenesis & Malignant transformation. The author has an hindex of 11, co-authored 12 publications receiving 452 citations. Previous affiliations of Jin Dai include The Graduate Center, CUNY.
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Journal ArticleDOI
Luteolin inhibits Cr(VI)-induced malignant cell transformation of human lung epithelial cells by targeting ROS mediated multiple cell signaling pathways.
Poyil Pratheeshkumar,Young-Ok Son,Sasidharan Padmaja Divya,Ram Vinod Roy,John Andrew Hitron,Lei Wang,Donghern Kim,Jin Dai,Padmaja Asha,Zhuo Zhang,Yitao Wang,Xianglin Shi +11 more
TL;DR: The results indicate that luteolin protects BEAS-2B cells from Cr(VI)-induced carcinogenesis by scavenging ROS and modulating multiple cell signaling mechanisms that are linked to ROS.
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Arsenic Induces Insulin Resistance in Mouse Adipocytes and Myotubes Via Oxidative Stress-Regulated Mitochondrial Sirt3-FOXO3a Signaling Pathway.
Sasidharan Padmaja Divya,Poyil Pratheeshkumar,Young-Ok Son,Ram Vinod Roy,John Andrew Hitron,Donghern Kim,Jin Dai,Lei Wang,Padmaja Asha,Bin Huang,Mei Xu,Jia Luo,Zhuo Zhang +12 more
TL;DR: The results show that chronic arsenic exposure significantly decreased insulin-stimulated glucose uptake (ISGU) in correlation with reduced expression of insulin-regulated glucose transporter type 4 (Glut4) and suggest that Sirt3/FOXO3a/MnSOD signaling plays a significant role in the inhibition of ISGU induced by chronic arsenic Exposure.
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Human bronchial epithelial BEAS-2B cells, an appropriate in vitro model to study heavy metals induced carcinogenesis.
TL;DR: Activity and expression of 53 and its downstream target protein p21 upon acute or chronic exposure of BEAS-2B cells to arsenic and Cr(VI) are examined, demonstrating that p53 is able to respond to exposure of arsenic or Cr( VI), suggesting that BEas- 2B cells are an appropriate in vitro model to investigate arsenic orCr( VI) induced lung cancer.
Journal ArticleDOI
Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signaling pathways in SKH-1 mice skin.
Sasidharan Padmaja Divya,Xin Wang,Poyil Pratheeshkumar,Young-Ok Son,Ram Vinod Roy,Donghern Kim,Jin Dai,John Andrew Hitron,Lei Wang,Padmaja Asha,Xianglin Shi,Zhuo Zhang +11 more
TL;DR: Blackberry extract protects from UVB-induced oxidative damage and inflammation by modulating MAP kinase and NF-κB signaling pathways, and results show that BBE suppressedUVB- induced hyperplasia and reduced infiltration of inflammatory cells in the SKH-1 hairless mice skin.
Journal ArticleDOI
Quercetin inhibits Cr(VI)-induced malignant cell transformation by targeting miR-21-PDCD4 signaling pathway.
Poyil Pratheeshkumar,Young-Ok Son,Sasidharan Padmaja Divya,Lei Wang,Lilia Turcios,Ram Vinod Roy,John Andrew Hitron,Donghern Kim,Jin Dai,Padmaja Asha,Zhuo Zhang,Xianglin Shi +11 more
TL;DR: Results demonstrate that quercetin is able to protect BEAS-2B cells from Cr(VI)-induced carcinogenesis by targeting miR-21-PDCD4 signaling.