Inhibition of SNCG suppresses the proliferation of lung cancer cells induced by high glucose.

Abstract

Lung cancer is the most common cancer type worldwide and the leading cause of cancer-related mortality. Diabetes is closely associated with the occurrence, development and prognosis of lung cancer. Therefore, the present study aimed to investigate whether SNCG could affect the proliferation of lung cancer cells induced by high glucose. Lung cancer cells induced by high glucose simulated the pathologies of patients with lung cancer with diabetes in vitro. The proliferation of HBE cells and lung cancer cells after transfection and treatment of glucose was detected using Cell Counting Kit-8 assay. The mRNA expression levels of synuclein γ (SNCG), insulin-like growth factor 1 (IGF-1) and IGF-1 receptor (IGF-1R) in HBE cells and lung cancer cells alone, or cells induced by high glucose were analyzed via reverse transcription-quantitative (RT-q)PCR analysis. Moreover RT-qPCR analysis was used to determine the transfection efficiencies. The clone formation ability, migration and inflammation of lung cancer cells after high glucose induction and transfection were detected using clone formation, wound healing and ELISA assays. The protein expression levels of SNCG, IGF-1, IGF-1R, ERK 1/2, phosphorylated (p)-ERK1/2 and JNK in lung cancer cells after high glucose induction and transfection were determined using western blot analysis. The results suggested that high glucose significantly promoted the proliferation of A549, NCI-H1975 and SK-MES-1 cells at 24 and 48 h, as well as upregulated the expression levels of SNCG, IGF-1 and IGF-1R. Knockdown of SNCG suppressed the proliferation, clone formation ability and migration, but alleviated inflammation in A549 cells induced by high glucose. Knockdown of SNCG suppressed the expression levels of SNCG, IGF-1, IGF-1R, ERK1/2 and p-ERK1/2, while it promoted JNK expression in A549 cells induced by high glucose. The effect of AXL1717 (an IGF-1R inhibitor) treatment on cells was consistent with that of SNCG knockdown. In conclusion, inhibition of SNCG suppresses proliferation of lung cancer cells induced by high glucose.

• Authors: Jing Fei, Chi Xiao, Meiying Yang, Xue Zhou, Ping Gong
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 23 Issue 2 (02 2021) ISSN: 1791-3004 [Electronic] Greece
• PMID: 33313952 (Publication Type: Journal Article)

Chemical References

• IGF1 protein, human
• IGF1R protein, human
• IL6 protein, human
• Interleukin-6
• Neoplasm Proteins
• SNCG protein, human
• TNF protein, human
• Tumor Necrosis Factor-alpha
• gamma-Synuclein
• picropodophyllin
• Insulin-Like Growth Factor I
• Receptor, IGF Type 1
• JNK Mitogen-Activated Protein Kinases
• MAPK1 protein, human
• MAPK3 protein, human
• Mitogen-Activated Protein Kinase 1
• Mitogen-Activated Protein Kinase 3
• Glucose
• Podophyllotoxin

Topics

• Cell Line, Tumor
• Cell Movement (drug effects, genetics)
• Cell Proliferation (genetics)
• Gene Knockdown Techniques
• Glucose (pharmacology)
• Humans
• Inflammation (chemically induced, genetics)
• Insulin-Like Growth Factor I (genetics, metabolism)
• Interleukin-6 (metabolism)
• JNK Mitogen-Activated Protein Kinases (metabolism)
• Lung Neoplasms (genetics, metabolism)
• Mitogen-Activated Protein Kinase 1 (metabolism)
• Mitogen-Activated Protein Kinase 3 (metabolism)
• Neoplasm Proteins (antagonists & inhibitors, genetics, metabolism)
• Podophyllotoxin (analogs & derivatives, pharmacology)
• Receptor, IGF Type 1 (antagonists & inhibitors, genetics, metabolism)
• Tumor Necrosis Factor-alpha (metabolism)
• Tumor Stem Cell Assay
• gamma-Synuclein (antagonists & inhibitors, genetics, metabolism)