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Ming Shi

Researcher at Academy of Military Medical Sciences

Publications -  41
Citations -  1451

Ming Shi is an academic researcher from Academy of Military Medical Sciences. The author has contributed to research in topics: Cancer cell & Cancer. The author has an hindex of 21, co-authored 40 publications receiving 1260 citations.

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Stat3-coordinated Lin-28-let-7-HMGA2 and miR-200-ZEB1 circuits initiate and maintain oncostatin M-driven epithelial-mesenchymal transition.

TL;DR: It is shown that oncostatin M (OSM) is expressed in an autocrine/paracrine fashion in invasive breast carcinoma and the importance of Stat3-coordinated Lin-28B–let-7–HMGA2 and miR-200–ZEB1 circuits in the cytokine-mediated phenotypic reprogramming of breast cancer cells is highlighted.
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The β2-adrenergic receptor and Her2 comprise a positive feedback loop in human breast cancer cells

TL;DR: The data indicate that Her2 overexpression and excessive phosphorylation of ERK cause epinephrine autocrine release from breast cancer cells, resulting in up-regulation of β2-AR expression, which supports a model where β1-AR and Her2 comprise a positive feedback loop in human Breast cancer cells.
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Acquisition of resistance to trastuzumab in gastric cancer cells is associated with activation of IL-6/STAT3/Jagged-1/Notch positive feedback loop

TL;DR: It is implicate that the IL-6/STAT3/Jagged-1/Notch axis may be a useful target and that combination of the Notch or STAT3 inhibitors with trastuzumab may prevent or delay clinical resistance and improve the efficacy of trastzumab in gastric cancer.
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Fra-1 and Stat3 synergistically regulate activation of human MMP-9 gene.

TL;DR: The study demonstrated that the activation of MMP-9 promoter is dependent upon interactions of Fra-1/c-Jun with Stat3, and a juxtaposed Stat3/AP-1 element plays a crucial role in the manner of enhancersome in theactivation of M MP-9 gene.
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Glucocorticoid regulation of a novel HPV–E6–p53–miR‐145 pathway modulates invasion and therapy resistance of cervical cancer cells

TL;DR: The findings identify a novel pathway through which the neuroendocrine macroenvironment affects cervical tumour growth, invasion and therapy resistance and show that miR‐145 may serve as a target for cervical cancer therapy.