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Xiaoxi Lv

Researcher at Peking Union Medical College

Publications -  45
Citations -  1121

Xiaoxi Lv is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Autophagy & Pulmonary fibrosis. The author has an hindex of 14, co-authored 39 publications receiving 673 citations. Previous affiliations of Xiaoxi Lv include Capital Medical University.

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DEDD Interacts with PI3KC3 to Activate Autophagy and Attenuate Epithelial–Mesenchymal Transition in Human Breast Cancer

TL;DR: It is shown that death-effector domain-containing DNA-binding protein (DEDD) attenuates EMT and acts as an endogenous suppressor of tumor growth and metastasis, and expression levels of DEDD were conversely correlated with poor prognosis in patients with breast and colon cancer.
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TRIB3 supports breast cancer stemness by suppressing FOXO1 degradation and enhancing SOX2 transcription

TL;DR: It is reported that expression of the pseudokinase Tribble 3 (TRIB3) positively associates with breast cancer stemness and progression and is a potential therapeutic strategy against TRIB3-overexpressed breast cancer.
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TRIB3 Interacts With β-Catenin and TCF4 to Increase Stem Cell Features of Colorectal Cancer Stem Cells and Tumorigenesis

TL;DR: This investigation investigated whether increased TRIB3 expression promotes stem cell features of CRC cells and tumor progression by interacting with the Wnt signaling pathway and derived organoids from human and mouse colorectal tumors to analyze the function of TRIB 3 and test the effect of a peptide inhibitor.
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TRIB3 Promotes APL Progression through Stabilization of the Oncoprotein PML-RARα and Inhibition of p53-Mediated Senescence

TL;DR: It is reported that expression of pseudokinase Tribble 3 (TRIB3) associates positively with APL progression and therapeutic resistance, and a potential therapeutic option against APL is provided.
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Disrupting the TRIB3-SQSTM1 interaction reduces liver fibrosis by restoring autophagy and suppressing exosome-mediated HSC activation

TL;DR: Together, stress-elevated TRIB3 expression promotes hepatic fibrosis by interacting with SQSTM1 and interfering with its functions in liver-parenchymal cells and activating HSCs, and targeting this interaction is a promising strategy for treating fibroproliferative liver diseases.