C
Cheng Wang
Researcher at National University of Singapore
Publications - 4
Citations - 434
Cheng Wang is an academic researcher from National University of Singapore. The author has contributed to research in topics: Drug resistance & Acetylation. The author has an hindex of 3, co-authored 4 publications receiving 175 citations.
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Journal ArticleDOI
Microglia-mediated neuroinflammation in neurodegenerative diseases.
TL;DR: This review gives a detailed account of the microglia-mediated neuroinflammation in various neurodegenerative diseases and shows great promise as a novel treatment strategy to reduce neuronal damage and to foster a permissive environment for further regeneration effort.
Journal ArticleDOI
SRPK1 acetylation modulates alternative splicing to regulate cisplatin resistance in breast cancer cells.
Cheng Wang,Zhihong Zhou,Charannya Sozheesvari Subhramanyam,Qiong Cao,Zealyn Shi Lin Heng,Wen Liu,Xiang-Dong Fu,Qidong Hu +7 more
TL;DR: This study reveals a key role of SRPK1 in the development of cisplatin resistance in breast cancer cells and suggests a potential therapeutic avenue for overcoming chemotherapy resistance and identifies a potential strategy to treat cancers resistant to platinum-based therapy.
Journal ArticleDOI
Role of PIWI-like 4 in modulating neuronal differentiation from human embryonal carcinoma cells
Charannya Sozheesvari Subhramanyam,Qiong Cao,Cheng Wang,Zealyn Shi Lin Heng,Zhihong Zhou,Qidong Hu +5 more
TL;DR: A novel somatic role of PIWIL4 in modulating the expression of neuronal genes that can be further characterized to promote neuronal differentiation and to modulate the activity of glioma cells is suggested.
Journal ArticleDOI
The role of 17β‑estradiol‑induced upregulation of Piwi‑like 4 in modulating gene expression and motility in breast cancer cells.
Zealyn Shi Lin Heng,Jing Yi Lee,Charannya Sozheesvari Subhramanyam,Cheng Wang,Lal Zo Thanga,Qidong Hu +5 more
TL;DR: Piwil4 is a novel regulator of ER signaling that could be targeted to inhibit breast cancer growth and migration and the loss-of-function of Piwil4 reduced the motility of MCF-7 cells in wound-healing assays, which could be associated to decreased expression of vimentin and N-cadherin.