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Multidimensional Coculture System to Model Lung Squamous Carcinoma Progression
Published on: March 17, 2020
Potential anti-cancer effect of curcumin in human lung squamous cell carcinoma
Wei Zhao1, Yan Wang1, Ying Wang2
1Thoracic Surgery Department, Third Hospital of Jilin University Changchun City, China.
Background:
To explore the molecular mechanisms of the anti-cancer effect of curcumin in human lung squamous cell carcinoma (LSQCC) SK-MES-1 cells.
Methods:
Cell viability was determined using MTT assay. Ribonucleic acid sequencing was performed to measure expression levels of transcripts in LSQCC cells treated with 15 μmol/L curcumin (treatment groups) or an equal amount of dimethylsulfoxide (control). Cuffdiff software was used to identify differentially expressed genes (DEGs) in treatment groups, followed by enrichment analysis of DEGs using the Database for Annotation, Visualization and Integration Discovery. The protein-protein interaction (PPI) networks for up and downregulated DEGs were constructed by Cytoscape software using Search Tool for the Retrieval of Interacting Genes data to identify hub nodes.
Results:
Curcumin significantly reduced cell viability in LSQCC cells. In total, 380 DEGs including 154 upregulated and 126 downregulated genes were found in the treatment groups. The upregulated genes were enriched in base excision repair (BER, such as PCNA, POLL, and MUTYH) and Janus kinase-signal transducer and activator of transcription (JAT-STAT) signaling pathways (such as AKT1 and STAT5A), while the downregulated genes were enriched in nine pathways, including the vascular endothelial growth factor (VEGF) signaling pathway (such as PTK2, VEGFA, MAPK1, and MAPK14) and mitogen-activated protein kinase (MAPK) signaling pathway (ARRB2, MAPK1, MAPK14, and NFKB1). PCNA and AKT1 were the hub nodes in the PPI network of upregulated genes while MAPK1, MAPK14, VEGFA, and NFKB1 were the hub nodes in the PPI network of downregulated genes.
Conclusions:
Curcumin might exert anti-cancer effects on LSQCC via regulating BER, JAT-STAT, VEGF, and MAPK signaling pathways.
Insights
Curcumin, a natural compound, significantly inhibits lung squamous cell carcinoma (LSQCC) growth by altering gene expression. It impacts key pathways including base excision repair (BER) and vascular endothelial growth factor (VEGF) signaling.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Lung squamous cell carcinoma (LSQCC) is a major subtype of non-small cell lung cancer.
- Understanding the molecular underpinnings of anti-cancer agents is crucial for developing targeted therapies.
- Curcumin, a polyphenol from turmeric, exhibits potential anti-cancer properties.
Purpose of the Study:
- To investigate the molecular mechanisms behind curcumin's anti-cancer effects in human LSQCC SK-MES-1 cells.
- To identify key signaling pathways and genes modulated by curcumin treatment.
Main Methods:
- Cell viability was assessed using MTT assays.
- RNA sequencing identified differentially expressed genes (DEGs) between curcumin-treated and control LSQCC cells.
- Enrichment analysis and protein-protein interaction (PPI) network construction (using Database for Annotation, Visualization and Integration Discovery and Cytoscape) elucidated pathway involvement and hub genes.
Main Results:
- Curcumin significantly reduced LSQCC cell viability.
- A total of 380 DEGs were identified, including 154 upregulated and 126 downregulated genes.
- Upregulated genes were enriched in base excision repair (BER) and Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathways. Downregulated genes were enriched in vascular endothelial growth factor (VEGF) and mitogen-activated protein kinase (MAPK) signaling pathways. PCNA, AKT1, MAPK1, MAPK14, VEGFA, and NFKB1 emerged as key hub nodes.
Conclusions:
- Curcumin demonstrates anti-cancer activity against LSQCC.
- The anti-cancer effects are potentially mediated through the regulation of BER, JAK-STAT, VEGF, and MAPK signaling pathways.
- Identifying these pathways provides insights into novel therapeutic strategies for LSQCC.
