scispace - formally typeset
W

Wei Gong

Researcher at Third Military Medical University

Publications -  17
Citations -  703

Wei Gong is an academic researcher from Third Military Medical University. The author has contributed to research in topics: Downregulation and upregulation & Regulation of gene expression. The author has an hindex of 11, co-authored 17 publications receiving 582 citations.

Papers
More filters
Journal ArticleDOI

LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells

TL;DR: The data reveals that the pathway ‘HULC/USP22/Sirt1/ protective autophagy’ attenuates the sensitivity of HCC cells to chemotherapeutic agents, suggesting that this pathway may be a novel target for developing sensitizing strategy to HCC chemotherapy.
Journal ArticleDOI

Curcumin Protects Against Collagen-Induced Arthritis via Suppression of BAFF Production

TL;DR: The results of the present study suggest that suppression of BAFF production may be a novel mechanism by which curcumin improves RA.
Journal ArticleDOI

FXR ligands protect against hepatocellular inflammation via SOCS3 induction

TL;DR: Modulation of SOCS3 expression may represent a novel mechanism through which FXR activation could selectively affect cytokine bioactivity in inflammation response.
Journal ArticleDOI

Upregulation of microRNA-122 by farnesoid X receptor suppresses the growth of hepatocellular carcinoma cells

TL;DR: Functional experiments showed that the FXR-mediated upregulation of miR-122 suppressed the proliferation of HCC cells in vitro and the growth of H CC xenografts in vivo, suggesting that FXR may serve as a key transcriptional regulator for manipulating mi R-122 expression, and theFXR/miR- 122 pathway may therefore be a novel target for the treatment of Hcc.
Journal ArticleDOI

LXRα-mediated downregulation of FOXM1 suppresses the proliferation of hepatocellular carcinoma cells.

TL;DR: It is demonstrated that specific LXRs agonists downregulated expression of FOXM1, cyclin D1 and cyclin B1 in hepatocellular carcinoma (HCC) cells, which led to cell cycle and cell proliferation arrest, suggesting that the pathway may be a novel target for HCC treatment.