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C-Phycocyanin Suppresses Cell Proliferation and Promotes Apoptosis by Regulating the AMPK Pathway in NCL-H292 Non-Small Cell Lung Cancer Cells
H. Chaowen, H. Dongxuan, H. Dongsheng, P. Jianfeng, Y. Fan, C. Yahui, L. Xiaohua
Language English Country Czech Republic
Document type Journal Article
NLK
Free Medical Journals
from 2000
Freely Accessible Science Journals
from 2000
ProQuest Central
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 2000
- MeSH
- Adenosine Monophosphate pharmacology therapeutic use MeSH
- Annexin A5 pharmacology therapeutic use MeSH
- Apoptosis MeSH
- Phycocyanin metabolism pharmacology therapeutic use MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- Lung Neoplasms * drug therapy genetics metabolism MeSH
- Carcinoma, Non-Small-Cell Lung * drug therapy genetics metabolism MeSH
- Cell Movement MeSH
- Cell Proliferation MeSH
- AMP-Activated Protein Kinases genetics metabolism pharmacology MeSH
- RNA, Long Noncoding * genetics MeSH
- Sincalide metabolism pharmacology therapeutic use MeSH
- Sirolimus pharmacology therapeutic use MeSH
- TOR Serine-Threonine Kinases metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Non-small cell lung cancer (NSCLC) results in high mortality and has gained increasing attention. C-Phycocyanin (C-PC) has been identified as a potential therapeutic inhibitor for NSCLC, but its underlying mechanism remains obscure. The gene expression of the long noncoding RNA neighbour of BRCAI RNA 2 (NBR2) in NSCLC cells was evaluated by quantitative reverse transcription-PCR. The cell capacity for proliferation and migration was examined by EdU and wound-healing assays. Furthermore, the viability and apoptosis of cells was measured with CCK-8 and annexin V/PI, respectively. Next, the protein level of activation of adenosine monophosphate- activated protein kinase and the rapamycin kinase (mTOR) signalling pathway-associated molecules was evaluated by western blotting. H292 cells were pre-treated with C-PC or transfected with plasmids encoding NBR2 or the shNBR2 plasmid, to over-express or knock down NBR2 expression, respectively. NBR2 expression was robustly down-regulated in NSCLC cell lines compared with a normal cell line (BEAS-2B). NBR2 over-expression inhibited migration and promoted apoptosis of H292 cells. Treatment of H292 cells with C-PC enhanced NBR2 levels in a dose- and time-dependent manner. Downregulation of NBR2 in H292 cells inhibited the activity of C-PC on cell proliferation, viability and clone formation. Further mechanistic investigation showed that the down-regulation of NBR2 abolished the modulatory effects of C-PC on the AMPK/mTOR signalling pathway. In conclusion, C-PC inhibits H292 cell growth by enhancing the NBR2/AMPK signalling pathway.
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- $a Non-small cell lung cancer (NSCLC) results in high mortality and has gained increasing attention. C-Phycocyanin (C-PC) has been identified as a potential therapeutic inhibitor for NSCLC, but its underlying mechanism remains obscure. The gene expression of the long noncoding RNA neighbour of BRCAI RNA 2 (NBR2) in NSCLC cells was evaluated by quantitative reverse transcription-PCR. The cell capacity for proliferation and migration was examined by EdU and wound-healing assays. Furthermore, the viability and apoptosis of cells was measured with CCK-8 and annexin V/PI, respectively. Next, the protein level of activation of adenosine monophosphate- activated protein kinase and the rapamycin kinase (mTOR) signalling pathway-associated molecules was evaluated by western blotting. H292 cells were pre-treated with C-PC or transfected with plasmids encoding NBR2 or the shNBR2 plasmid, to over-express or knock down NBR2 expression, respectively. NBR2 expression was robustly down-regulated in NSCLC cell lines compared with a normal cell line (BEAS-2B). NBR2 over-expression inhibited migration and promoted apoptosis of H292 cells. Treatment of H292 cells with C-PC enhanced NBR2 levels in a dose- and time-dependent manner. Downregulation of NBR2 in H292 cells inhibited the activity of C-PC on cell proliferation, viability and clone formation. Further mechanistic investigation showed that the down-regulation of NBR2 abolished the modulatory effects of C-PC on the AMPK/mTOR signalling pathway. In conclusion, C-PC inhibits H292 cell growth by enhancing the NBR2/AMPK signalling pathway.
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