MiR-96-5p Suppresses Progression of Arsenite-Induced Human Keratinocyte Proliferation and Malignant Transformation by Targeting Denticleless E3 Ubiquitin Protein Ligase Homolog
Yan Li, Qiaoshi Zhao, Jinyin Yao, Chunpeng Lv, Yanhui Gao, Dianjun Sun, Yanmei Yang, Lisa J Bain · 2023
Read MiR-96-5p Suppresses Progression of Arsenite-Induced Human Keratinocyte Proliferation and Malignant Transformation by Targeting Denticleless E3 Ubiquitin Protein Ligase Homolog by Yan Li, Qiaoshi Zhao, Jinyin Yao, Chunpeng Lv, Yanhui Gao, Dianjun Sun, Yanmei Yang, Lisa J Bain (2023) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-10747408.txt.
Description
Yan Li and co-authors identify a small RNA standing guard against arsenic's slow march toward skin cancer. Chronic arsenic exposure is a proven cause of skin cancer, and molecular drivers are still being mapped. Mining expression data from arsenite-treated skin cells, the team zeroed in on miR-96-5p and its target, the ubiquitin ligase component DTL.
Arsenite lowered the protective RNA, freeing DTL to rise and drive growth and malignant change in the cultured cells. Restoring the RNA, or silencing DTL, reversed the effect. In mice, tumors grown from arsenite-transformed cells shrank when the RNA was replaced, with DTL falling in step. The authors propose the RNA-DTL axis as both a mechanism of arsenic carcinogenesis and a possible therapeutic handle.
Catalog record
| CREATOR | Yan Li, Qiaoshi Zhao, Jinyin Yao, Chunpeng Lv, Yanhui Gao, Dianjun Sun, Yanmei Yang, Lisa J Bain |
|---|---|
| YEAR | 2023 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 42 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |