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  4. Engineered bacteriorhodopsin may induce lung cancer cell cycle arrest and suppress their proliferation and migration
 
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Engineered bacteriorhodopsin may induce lung cancer cell cycle arrest and suppress their proliferation and migration

Journal
Molecules
Journal Volume
26
Journal Issue
23
Pages
Article number 7344
Date Issued
2021-12-01
Author(s)
Wong, Chui Wei
Ko, Ling Ning
Huang, Hung Jin
CHII-SHEN YANG  
SHAN-HUI HSU  
DOI
10.3390/molecules26237344
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/592525
URL
https://api.elsevier.com/content/abstract/scopus_id/85121140881
Abstract
Highly expressible bacteriorhodopsin (HEBR) is a light-triggered protein (optogenetic protein) that has seven transmembrane regions with retinal bound as their chromophore to sense light. HEBR has controllable photochemical properties and regulates activity on proton pumping. In this study, we generated HEBR protein and incubated with lung cancer cell lines (A549 and H1299) to evaluate if there was a growth-inhibitory effect with or without light illumination. The data revealed that the HEBR protein suppressed cell proliferation and induced the G0 /G1 cell cycle arrest without light illumination. Moreover, the migration abilities of A549 and H1299 cells were reduced by ~17% and ~31% after incubation with HEBR (40 µg/mL) for 4 h. The Snail-1 gene expression level of the A549 cells was significantly downregulated by ~50% after the treatment of HEBR. In addition, HEBR significantly inhibited the gene expression of Sox-2 and Oct-4 in H1299 cells. These results suggested that the HEBR protein may inhibit cell proliferation and cell cycle progression of lung cancer cells, reduce their migration activity, and suppress some stemness-related genes. These findings also suggested the potential of HEBR protein to regulate the growth and migration of tumor cells, which may offer the possibility for an anticancer drug.
Subjects
Cytotoxicity | Migration ability | Non-small cell lung cancer | Optogenetic protein | Proton pump
SDGs

[SDGs]SDG3

Publisher
MDPI
Type
journal article

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