Tobacco carcinogen NNK promotes pancreatic cancer proliferation via LINC00857/β-catenin
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View abstract on PubMed
Summary
This summary is machine-generated.Nicotine-derived nitrosamine ketone (NNK) from tobacco smoke promotes pancreatic cancer (PC) growth by upregulating LINC00857 and the β-catenin pathway. Smoking cessation is crucial for PC prevention.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Research
Background
- Smoking is a significant risk factor for pancreatic cancer (PC).
- Nicotine-derived nitrosamine ketone (NNK), a tobacco carcinogen, is implicated in cancer promotion, but its role in PC progression and regulation of long non-coding RNAs (lncRNAs) like LINC00857 is not fully understood.
Purpose Of The Study
- To investigate the role of NNK in driving PC growth.
- To elucidate the underlying molecular mechanisms, focusing on the regulation of LINC00857 and its potential downstream targets.
Main Methods
- Human PC cell lines (CFPAC-1, Panc-1) were treated with NNK.
- Cell proliferation was assessed using CCK-8, colony formation, and EdU assays.
- LINC00857 expression was analyzed via bioinformatic interrogation of public and institutional databases.
- LINC00857 knockdown was performed using siRNA.
- β-catenin expression was measured by Western blotting and qRT-PCR.
Main Results
- NNK exposure enhanced PC cell proliferation.
- LINC00857 was found to be upregulated in PC and correlated with smoking status.
- Knockdown of LINC00857 inhibited PC cell proliferation.
- NNK-induced upregulation of β-catenin was suppressed by LINC00857 knockdown at both protein and transcriptional levels.
Conclusions
- NNK may promote PC progression via the LINC00857/β-catenin signaling axis.
- These findings underscore the importance of smoking cessation in PC prevention strategies.
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