Y
Yong Teng
Researcher at Emory University
Publications - 166
Citations - 4478
Yong Teng is an academic researcher from Emory University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 31, co-authored 119 publications receiving 2609 citations. Previous affiliations of Yong Teng include Sun Yat-sen University & Chongqing University.
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Journal ArticleDOI
Is It Time to Start Transitioning From 2D to 3D Cell Culture
Caleb Jensen,Yong Teng +1 more
TL;DR: 3D cellculture has the potential to provide alternative ways to study organ behavior via the use of organoids and is expected to eventually bridge the gap between 2D cell culture and animal models.
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Evaluating human cancer cell metastasis in zebrafish
TL;DR: The zebrafish model offers a rapid, robust, and inexpensive means of evaluating the metastatic potential of human cancer cells and is possible to critically evaluate whether genetic manipulation of signaling pathways affects metastasis and whether primary tumors contain metastatic cells.
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Cancer-associated fibroblast (CAF)-derived IL32 promotes breast cancer cell invasion and metastasis via integrin β3-p38 MAPK signalling
Siyang Wen,Yixuan Hou,Lixin Fu,Lei Xi,Dan Yang,Maojia Zhao,Yilu Qin,Kexin Sun,Yong Teng,Manran Liu +9 more
TL;DR: It is found that interaction of interleukin 32 with integrin β3 mediating the cross-talk between CAFs and breast cancer cells plays a crucial role in CAF-induced breast tumour invasiveness and metastasis.
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FGF19/FGFR4 signaling contributes to the resistance of hepatocellular carcinoma to sorafenib
TL;DR: It is shown that targeting FGF19/FGFR4 axis by ponatinib, a third-generation inhibitor of chronic myeloid leukemia, overcomes HCC resistance of sorafenib by enhancing ROS-associated apoptosis in sorAFenib-treated HCC.
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The involvement of JAK-STAT3 in cell motility, invasion, and metastasis.
TL;DR: Better understanding of the complex role played by JAK-STAT3 in the regulation of cell movement, invasion, and metastasis provides opportunities to suppress this lethal aspect of cancer progression by not only targeting the JAK and STAT3 proteins directly, but also some of the downstream effectors of JAK -STAT3 signaling.