2. Academic Validation
  3. Lamin B2 promotes the malignant phenotype of non-small cell lung cancer cells by upregulating dimethylation of histone 3 lysine 9

Lamin B2 promotes the malignant phenotype of non-small cell lung cancer cells by upregulating dimethylation of histone 3 lysine 9

  • Exp Cell Res. 2020 Aug 15;393(2):112090. doi: 10.1016/j.yexcr.2020.112090.
Mei-Yu Zhang 1,  Yu-Chen Han 2,  Qiang Han 3,  Yuan Liang 4,  Yuan Luo 4,  Lai Wei 4,  Ting Yan 4,  Yue Yang 4,  Shu-Li Liu 5,  En-Hua Wang 6
Affiliations

Affiliations

  • 1 Department of Pathology, College of Basic Medical Sciences, China Medical University, China. Electronic address: [email protected].
  • 2 Department of Pathology, Shanghai Jiaotong University Affiliated Chest Hospital, China.
  • 3 Department of Pathology, College of Basic Medical Sciences, China Medical University, China; The First Affiliated Hospital of China Medical University, China.
  • 4 Department of Pathology, College of Basic Medical Sciences, China Medical University, China.
  • 5 Department of Pathology, College of Basic Medical Sciences, China Medical University, China; The First Affiliated Hospital of China Medical University, China. Electronic address: [email protected].
  • 6 Department of Pathology, College of Basic Medical Sciences, China Medical University, China; The First Affiliated Hospital of China Medical University, China. Electronic address: [email protected].
PMID: 32416090 DOI: 10.1016/j.yexcr.2020.112090
Abstract

The relationship between Lamin B2 and tumor proliferation and migration is unclear. We explored the impact of Lamin B2 on non-small cell lung Cancer (NSCLC) cells. Tissue microarray and immunohistochemistry were combined to evaluate Lamin B2 expression and its relationship with the clinicopathological factors found in NSCLC. Western blotting, immunofluorescence analysis, and bioinformatics were used to investigate the effects of Lamin B2 on various regulatory pathways in Cancer. Cytological experiments were conducted to evaluate Lamin B2 expression in tumor cells. We conducted co-immunoprecipitation and chromatin immunoprecipitation to explore the molecular mechanisms underlying the relationship between Lamin B2 and NSCLC and evaluate the results of rescue experiments. Lamin B2 was highly expressed in NSCLC and positively correlated with lymph node metastasis. In NSCLC, Lamin B2 interacted with Cyclin D1, upregulating G9α expression, thus increasing H3K9me2 levels. H3K9me2 binds to the promoter region of the E-cadherin gene (CDH1) to induce CDH1 silencing and promotes Cancer cell migration. Thus, we found that Lamin B2 was highly expressed in NSCLC cells and promoted their migration by increasing H3K9me2 levels, which induced E-cadherin gene silencing.

Keywords

Epigenetic; H3K9me2; Lamin B2; Migration; Non-small cell lung cancer.

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