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C-Phycocyanin Suppresses Cell Proliferation and Promotes Apoptosis by Regulating the AMPK Pathway in NCL-H292
H Chaowen1, H Dongxuan1, H Dongsheng1
1Department of Pulmonary and Critical Care Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, China.
Abstract:
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.
Insights
C-Phycocyanin (C-PC) inhibits non-small cell lung cancer (NSCLC) growth by boosting NBR2 expression. This mechanism involves the NBR2/AMPK signaling pathway, offering a new therapeutic strategy for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality.
- C-Phycocyanin (C-PC) shows therapeutic potential against NSCLC, but its mechanism is unclear.
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression.
Purpose of the Study:
- To investigate the mechanism by which C-Phycocyanin (C-PC) inhibits NSCLC growth.
- To evaluate the role of the long noncoding RNA NBR2 in NSCLC and its interaction with C-PC.
- To elucidate the involvement of the AMPK/mTOR signaling pathway in C-PC's anti-cancer effects.
Main Methods:
- Quantitative reverse transcription-PCR (qRT-PCR) to measure NBR2 gene expression.
- Cell proliferation (EdU), migration (wound-healing), viability (CCK-8), and apoptosis (Annexin V/PI) assays.
- Western blotting to assess protein levels in the AMPK/mTOR pathway.
- Overexpression and knockdown of NBR2 using plasmids and shRNA in H292 NSCLC cells.
Main Results:
- NBR2 expression was significantly downregulated in NSCLC cell lines compared to normal cells.
- Overexpression of NBR2 inhibited H292 cell migration and promoted apoptosis.
- C-PC treatment increased NBR2 levels in a dose- and time-dependent manner.
- C-PC's inhibitory effects on proliferation, viability, and clone formation were dependent on NBR2 expression.
- Downregulation of NBR2 abolished C-PC's effects on the AMPK/mTOR pathway.
Conclusions:
- C-Phycocyanin (C-PC) inhibits non-small cell lung cancer (NSCLC) cell growth.
- The mechanism involves the upregulation of NBR2 expression.
- This effect is mediated through the NBR2/AMPK signaling pathway, highlighting a potential therapeutic target.
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