C-Phycocyanin Suppresses Cell Proliferation and Promotes Apoptosis by Regulating the AMPK Pathway in NCL-H292 Non-Small Cell Lung Cancer Cells
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
36201854
DOI
10.14712/fb2022068010016
PII: file/6210/fb2022a0002.pdf
Knihovny.cz E-zdroje
- MeSH
- adenosinmonofosfát farmakologie terapeutické užití MeSH
- annexin A5 farmakologie terapeutické užití MeSH
- apoptóza MeSH
- fykokyanin metabolismus farmakologie terapeutické užití MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádory plic * farmakoterapie genetika metabolismus MeSH
- nemalobuněčný karcinom plic * farmakoterapie genetika metabolismus MeSH
- pohyb buněk MeSH
- proliferace buněk MeSH
- proteinkinasy aktivované AMP genetika metabolismus farmakologie MeSH
- RNA dlouhá nekódující * genetika MeSH
- sinkalid metabolismus farmakologie terapeutické užití MeSH
- sirolimus farmakologie terapeutické užití MeSH
- TOR serin-threoninkinasy metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adenosinmonofosfát MeSH
- annexin A5 MeSH
- fykokyanin MeSH
- proteinkinasy aktivované AMP MeSH
- RNA dlouhá nekódující * MeSH
- sinkalid MeSH
- sirolimus MeSH
- TOR serin-threoninkinasy 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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