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Jiayuh Lin

Researcher at The Research Institute at Nationwide Children's Hospital

Publications -  88
Citations -  6224

Jiayuh Lin is an academic researcher from The Research Institute at Nationwide Children's Hospital. The author has contributed to research in topics: STAT3 & Phosphorylation. The author has an hindex of 44, co-authored 83 publications receiving 5789 citations. Previous affiliations of Jiayuh Lin include University of Michigan & Ohio State University.

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A low-molecular-weight compound discovered through virtual database screening inhibits Stat3 function in breast cancer cells

TL;DR: Investigation demonstrated that STA-21 inhibits Stat3 DNA binding activity, Stat3 dimerization, and Stat3-dependent luciferase activity, and reduces the survival of breast carcinoma cells with constitutive Stat3 signaling but has minimal effect on the cells in which constitutive stat3 signaling is absent.
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Curcumin is a potent DNA hypomethylation agent.

TL;DR: Curcumin inhibits the activity of M. SssI with an IC(50) of 30 nM, but no inhibitory activity of hexahydrocurcumin up to 100 microM, and can induce global DNA hypomethylation in a leukemia cell line.
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Inhibition of constitutively active Stat3 suppresses growth of human ovarian and breast cancer cells

TL;DR: It is shown that inhibition of the Stat3 signaling pathway using the Janus Kinase-selective inhibitor, AG490, and a dominant negative Stat3 (Stat3β) significantly suppresses the growth of ovarian and breast cancer cell lines harboring constitutively active Stat3.
Journal Article

Overexpression of Akt/AKT can modulate chemotherapy-induced apoptosis.

TL;DR: Results suggest that Akt/AKT1 expressed in these clones can phosphorylate Bad and prevent it from binding to Bcl-XL and provide evidence that aberrant expression or activation of AKT in cancer cells may confer resistance to paclitaxel.
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Novel STAT3 Phosphorylation Inhibitors Exhibit Potent Growth-Suppressive Activity in Pancreatic and Breast Cancer Cells

TL;DR: FLLL31 and FLLL32 are effective inhibitors of STAT3 phosphorylation, DNA-binding activity, and transactivation in vitro, leading to the impediment of multiple oncogenic processes and the induction of apoptosis in pancreatic and breast cancer cell lines.