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Ning Guo

Researcher at Academy of Military Medical Sciences

Publications -  41
Citations -  1697

Ning Guo 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 22, co-authored 41 publications receiving 1444 citations. Previous affiliations of Ning Guo include Henan University.

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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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A new format of bispecific antibody: highly efficient heterodimerization, expression and tumor cell lysis.

TL;DR: A new format of BsAb that consists of two single-chain variable fragment of antibodies, one for human epidermal growth factor receptor 2 (HER2)/neu and the other for CD16, heterodimerized by a "knobs-into-holes" device from the CH3 domains of the human IgG1 Fc fragment is described.
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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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Chronic psychological stress promotes lung metastatic colonization of circulating breast cancer cells by decorating a pre-metastatic niche through activating β-adrenergic signaling.

TL;DR: It is demonstrated that disturbance of host macro‐environmental homeostasis has an influence on future metastatic organs and stress‐related catecholamine may act as a crucial factor in regulating the pre‐metastatic niche for and lung colonization by tumor cells.