Wei Tan

Dr. Wei Tan


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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19 November 2019 in Journal of Cellular Physiology
Verified
Journal Article
Closed access
PDF file
ZWZhenting Wang
Zhenting Wang
QLQing Liu
Qing Liu
CLCongcong Liu
Congcong Liu
WTWei Tan
Wei Tan
MTMingying Tang
Mingying Tang
YDYouwen Deng
Youwen Deng

1 July 2024 in Bioactive Materials
Verified
Journal Article
Open access
HZHao Zhou
Hao Zhou
JHJinpeng He
Jinpeng He
RLRenfeng Liu
Renfeng Liu
JCJun Cheng
Jun Cheng
YYYuhao Yuan
Yuhao Yuan
YDYouwen Deng
Youwen Deng
Intervertebral disc degeneration (IVDD) can be caused by aging, injury, and genetic factors. The pathological changes associated with IVDD include the excessive accumulation of reactive oxygen species (ROS), cellular pyroptosis, and extracellular matrix (ECM) degradation. There are currently no approved specific molecular therapies for IVDD. In this study, we developed a multifunctional and microenvironment-responsive metal-phenolic network release platform, termed TMP@Alg-PBA/PVA, which could treat (IL-1β)-induced IVDD. The metal-phenolic network (TA-Mn-PVP, TMP) released from this platform targeted mitochondria to efficiently scavenge ROS and reduce ECM degradation. Pyroptosis was suppressed through the inhibition of the IL-17/ERK signaling pathway. These findings demonstrate the versatility of the platform. And in a rat model of IVDD, TMP@Alg-PBA/PVA exhibited excellent therapeutic effects by reducing the progression of the disease. TMP@Alg-PBA/PVA, therefore, presents clinical potential for the treatment of IVDD.

1 January 2021 in Materials Science and Engineering: C
Verified
Journal Article
Closed access
WTWei Tan
Wei Tan
Chengde GaoChengde Gao
Chengde Gao
PFPei Feng
Pei Feng
QLQing Liu
Qing Liu
CLCongcong Liu
Congcong Liu
CSCijun Shuai
Cijun Shuai

10 October 2019 in Cell Cycle
Verified
Journal Article
Closed access
QLQing Liu
Qing Liu
ZWZhenting Wang
Zhenting Wang
XZXiaohua Zhou
Xiaohua Zhou
MTMingying Tang
Mingying Tang
WTWei Tan
Wei Tan
YDYouwen Deng
Youwen Deng
Osteosarcoma (OS) accounts for 9 percent of cancer-related deaths in young people. The PI3K/Akt signaling, a well-known carcinogenic signaling pathway in human cancer, cooperates with other signaling pathways such as Wnt signaling to promote cancer progression. Wnt7b, as a transforming member of the Wnt family, could activate mTORC1 through PI3K-AKT signaling and is upregulated in OS. In the present study, we found that miR-342-5p inhibits Wnt7b expression via direct binding to Wnt7b 3′-UTR. miR-342-5p overexpression remarkably suppressed the viability and invasion while enhanced the apoptosis of OS cells; meanwhile, Wnt7b, β-catenin, c-myc, and cyclin D1 proteins were reduced while E-cadherin protein showed to be increased. Consistent with its expression pattern, Wnt7b exerted oncogenic effects on OS cells. Wnt7b could significantly attenuate the impacts of miR-342-5p. In conclusion, we demonstrated a miR-342-5p/Wnt7b axis that regulates the capacity of OS cells to proliferate and to invade through Wnt/β-catenin signaling. The miR-342-5p/Wnt7b axis might be novel targets for OS targeted therapy, which needs further in vivo and clinical investigations.

4 July 2016 in Cellular Oncology
Verified
Journal Article
Closed access
PDF file
CZChusong Zhou
Chusong Zhou
WTWei Tan
Wei Tan
HLHai Lv
Hai Lv
FGFei Gao
Fei Gao
JSJin Sun
Jin Sun

4 June 2023 in Small
Verified
Journal Article
Closed access
ZYZuyun Yan
Zuyun Yan
TSTianshi Sun
Tianshi Sun
WTWei Tan
Wei Tan
ZWZhicheng Wang
Zhicheng Wang
JYJinpeng Yan
Jinpeng Yan
YDYouwen Deng
Youwen Deng