ArticleOncotarget2017
Lamin B2 binding to minichromosome maintenance complex component 7 promotes non-small cell lung carcinogenesis.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Extracellular transfer of HuR promotes acquired cisplatin resistance in esophageal cancer cells.Cancer biology & therapy · 2025Article
- Review
- miR-656-3p inhibits melanomas in vitro and in vivo by inducing senescence via inhibiting LMNB2.Journal of cancer research and clinical oncology · 2023Article
- Lamin B2 contributes to the proliferation of bladder cancer cells via activating the expression of cell division cycle‑associated protein 3.International journal of molecular medicine · 2022Article
- Combined Transcriptomic and Proteomic Profiling to Unravel Osimertinib, CARP-1 Functional Mimetic (CFM 4.17) Formulation and Telmisartan Combo Treatment in NSCLC Tumor Xenografts.Pharmaceutics · 2022Article
- Kruppel like factor 16 promotes lung adenocarcinoma progression by upregulating lamin B2.Bioengineered · 2022Article
- MS275 as Class I HDAC inhibitor displayed therapeutic potential on malignant ascites by iTRAQ-based quantitative proteomic analysis.BMC gastroenterology · 2022Article
- LMNB2 promotes the progression of colorectal cancer by silencing p21 expression.Cell death & disease · 2021Article
- Long Noncoding RNAFrontiers in oncology · 2021Article
- miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2.Oncology research · 2020Article
- Construction and Analysis of lncRNA-Mediated ceRNA Network in Nasopharyngeal Carcinoma Based on Weighted Correlation Network Analysis.BioMed research international · 2020Article
- Amplification of Stem Genes: New Potential Metastatic Makers in Patients with an Early Form of Breast Cancer.Journal of Korean medical science · 2019Article
- MicroRNA-215-5p Treatment Suppresses Mesothelioma Progression via the MDM2-p53-Signaling Axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Dual strands of the miR-145 duplex (miR-145-5p and miR-145-3p) regulate oncogenes in lung adenocarcinoma pathogenesis.Journal of human genetics · 2018Article
- The plasma peptides of ovarian cancer.Clinical proteomics · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of lamin B2 in non-small cell lung cancer (NSCLC). We detected higher lamin B2 expression in 20 NSCLC tumor tissues obtained from The Cancer Genome Atlas than in adjacent normal lung tissues. LMNB2-RNAi knockdown in A549 and H1299 NSCLC cells inhibited colony formation, cell proliferation and G1-S cell cycle progression while increasing apoptosis. LMNB2 overexpression had the opposite effects. Tumor xenograft experiments showed diminished tumor growth with LMNB2 knockdown H1299 cells than with controls. Yeast two-hybrid studies revealed minichromosome maintenance complex component 7 (MCM7) to be a binding partner of lamin B2, which was confirmed by co-immunoprecipitation and co-localization studies. Lamin B2 binding enhanced DNA binding and helicase activities of MCM7. Deletion analysis with MCM7-N, MCM7-M or MCM7-C mutant proteins showed that lamin B2 binds to the C-terminus of MCM7, and competes with the binding of the tumor suppressor retinoblastoma (RB) protein. Immunohistochemical analysis of 150 NSCLC patient samples revealed that both lamin B2 and MCM7 levels positively correlated with histological grade and tumor TNM stage. Moreover, high lamin B2 and MCM7 levels correlated with shorter overall survival of NSCLC patients. In sum, these results show that lamin B2 interaction with MCM7 promotes NSCLC progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.