Carcinogenesis, Teratogenesis & Mutagenesis ›› 2018, Vol. 30 ›› Issue (3): 165-170,175.doi: 10.3969/j.issn.1004-616x.2018.03.001

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Inhibition of proliferation and migration of lung adenocarcinoma cells by SOX30 gene via regulation of DSC3 gene

MA Bangjing1, HAO Xianglin2, HAN Fei2, CHEN Hongqiang2, LIU Jinyi2, CAO Jia2, ZHANG Aihua1   

  1. 1. Toxicology Teaching and Research Section, School of Public Health, Guizhou Medical University, Guiyang 550004, Guizhou;
    2. Institute of Toxicology, College of Preventive Medicine, Army Medical University, Chongqing 400038, China
  • Received:2018-03-21 Revised:2018-04-23 Online:2018-05-30 Published:2018-05-30

Abstract: OBJECTIVE: To investigate interactions between SOX30 and DSC3 genes and their roles in the development of lung adenocarcinoma. METHODS: The GO enrichment analysis was used to screen possible downstream genes and pathways of SOX30 transcriptional regulation. The JASPAR database was used to predict the SOX30 transcription binding sites in the promoter region of DSC3. Expression data of SOX30 and DSC3 were downloaded from the TCGA database,and their relationships were evaluated using the Spearman rank correlation analysis. The reverse transcription-PCR was used to measure the mRNA levels of DSC3 in A549-SOX30+DSC3 miRNA stably transfected cells and the lung tissues of SOX30+/+,SOX30+/- and SOX30-/- mice. The colony formation and wound healing assays were used to confirm whether the inhibition of the proliferation and migration of SOX30 in A549 cells depended on the expression of DSC3 or not. RESULTS: The GO enrichment analysis shows the function of SOX30 gene was significantly related to the cell junction proteins,such as focal adhesion,anchoring junction,and adhesion junction. And several SOX30 binding sites were found in the promoter region of DSC3. Furthermore,expression of DSC3 was in positive correlation with that of SOX30 in human lung adenocarcinoma(r=0.154,P=0.000). In addition,the ectopic expression of SOX30 in A549 cell lines dramatically increased DSC3 mRNA level (P < 0.05),and knockout of SOX30 significantly decreased DSC3 mRNA level in lung tissues of SOX30-/- mice (P < 0.05). In addition,knockdown of DSC3 attenuated the inhibition effects of SOX30 on proliferation and migration in A549 cells (P < 0.05). CONCLUSION: SOX30 was a critical transcription factor in the expression regulation of DSC3,and DSC3 was an important downstream gene of SOX30. Therefore,SOX30-DSC3 may play an important role in the development of lung adenocarcinoma.

Key words: SOX30, DCS3, lung cancer, regulation, proliferation, migration

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