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Na Che

Researcher at Tianjin Medical University

Publications -  30
Citations -  990

Na Che is an academic researcher from Tianjin Medical University. The author has contributed to research in topics: Vasculogenic mimicry & Medicine. The author has an hindex of 14, co-authored 21 publications receiving 855 citations. Previous affiliations of Na Che include Tianjin Medical University General Hospital.

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Expression and functional significance of Twist1 in hepatocellular carcinoma: its role in vasculogenic mimicry.

TL;DR: Investigation of HCC as a VM and EMT model indicates that Twist1 induces HCC cell plasticity in VM cells more through the suppression of E‐cadherin expression and the induction of VE‐c cadherin up‐regulation than through the VM pattern in vivo and in a three‐dimensional in vitro system.
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Promotion of tumor cell metastasis and vasculogenic mimicry by way of transcription coactivation by Bcl-2 and Twist1: a study of hepatocellular carcinoma.

TL;DR: A novel function of Bcl‐2 in EMT induction is described, insight into tumor progression is provided, and the B cl‐2/Twist1 complex is implicate as a potential target for developing chemotherapeutics.
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Promotion of hepatocellular carcinoma metastasis through matrix metalloproteinase activation by epithelial‐mesenchymal transition regulator Twist1

TL;DR: It is indicated that Twist1 induces HCC invasion via increased activity in MMPs, leading to poor clinical prognoses, and a novel cogitation in Twist2, which has no effect on H CC invasion and metastasis.
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Slug promoted vasculogenic mimicry in hepatocellular carcinoma.

TL;DR: It is demonstrated that slug expression was associated with EMT and cancer stem cell (CSCs) phenotype in HCC patients and slug overexpression lead to the maintenance of CSCs phenotype and VM formation was demonstrated in vivo.
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Dickkopf-1-promoted vasculogenic mimicry in non-small cell lung cancer is associated with EMT and development of a cancer stem-like cell phenotype

TL;DR: In vivo animal studies demonstrated that DKK1 enhances the growth of transplanted human tumours cells, as well as increased VM formation, mesenthymal phenotypes and CSC properties, and it is felt that Dkk1 may represent a novel target of NSCLC therapy.