Jun Li
Nankai University
9 Papers
Jun Li is an academic researcher from Nankai University. The author has contributed to research in topics: Breast cancer & Cancer cell. The author has an hindex of 7, co-authored 9 publications. Previous affiliations of Jun Li include Scripps Research Institute.
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Papers
CD44ICD promotes breast cancer stemness via PFKFB4-mediated glucose metabolism.
Ruifang Gao,Dan Li,Jing Xun,Wei Zhou,Jun Li,Juan Wang,Chen Liu,Xiru Li,Wenzhi Shen,Huan Qiao,Dwayne G. Stupack,Na Luo,Na Luo +12 more
TL;DR: It is found that the shortest CD44 isoform ( CD44s) inhibits breast cancer stemness, whereas the cleaved product of CD44 (CD44ICD) promotes breast cancerstemness and therapies that target PFKFB4 (e.g., 5MPN therapy) may lead to improved outcomes for cancer patients.
TGIF2 promotes the progression of lung adenocarcinoma by bridging EGFR/RAS/ERK signaling to cancer cell stemness
Renle Du,Wenzhi Shen,Yi Liu,Wenjuan Gao,Wei Zhou,Jun Li,Shuangtao Zhao,Chong Chen,Yanan Chen,Yanan Chen,Yanhua Liu,Yanhua Liu,Peiqing Sun,Rong Xiang,Rong Xiang,Yi Shi,Yi Shi,Yunping Luo +17 more
TL;DR: It is reported that TGIF2 mediates the EGFR–RAS–ERK signaling pathway to enhance the stemness of lung adenocarcinoma (LUAD) cells and, therefore, promote the progression and metastasis of LUAD.
TLR4 Promotes Breast Cancer Metastasis via Akt/GSK3β/β-Catenin Pathway upon LPS Stimulation.
Jun Li,Jing Yin,Wenzhi Shen,Ruifang Gao,Yanhua Liu,Yanan Chen,Xiru Li,Chenghu Liu,Rong Xiang,Na Luo +9 more
TL;DR: The relationship between TLR4 activation by LPS and breast cancer using both in vitro and in vivo models is substantiated and the Akt/GSK3β/β‐catenin signal transduction pathway may serve as a viable clinical treatment target in breast cancer.
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Exosomal tetraspanins mediate cancer metastasis by altering host microenvironment
Jun Lu,Jun Li,Shuo Liu,Teng Wang,Alessandro Ianni,Eva Bober,Thomas Braun,Rong Xiang,Shijing Yue +8 more
TL;DR: How the cancer exosomal tetraspanin alters extracellular environment and regulates cancer metastasis is discussed, which is a key element for the target cell selection of exosomes uptake that may lead to the reprogramming of target cells.
MGAT3-mediated glycosylation of tetraspanin CD82 at asparagine 157 suppresses ovarian cancer metastasis by inhibiting the integrin signaling pathway.
Jun Li,Jiawen Xu,Luhan Li,Alessandro Ianni,Poonam Kumari,Shuo Liu,Peiqing Sun,Thomas Braun,Xiaoyue Tan,Rong Xiang,Shijing Yue +10 more
TL;DR: It is demonstrated that CD82 glycosylation at Asn157 is necessary for CD82-mediated inhibition of ovarian cancer cells migration and metastasis in vitro and in vivo and it is revealed that the Glycosyltransferase MGAT3 is responsible forCD82 gly cosylation in ovarian cancer Cells.
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