ArticleOncoTargets and therapy2018
Inhibition of NIPBL enhances the chemosensitivity of non-small-cell lung cancer cells via the DNA damage response and autophagy pathway.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- NIPBL-mediated RAD21 facilitates tumorigenicity by the PI3K pathway in non-small-cell lung cancer.Communications biology · 2024Article
- Solid-Tubulocystic carcinoma: A new variant of intrahepatic cholangiocarcinoma.World journal of hepatology · 2023Review
- Regulation of apoptosis, autophagy and ferroptosis by non-coding RNAs in metastatic non-small cell lung cancer (Review).Experimental and therapeutic medicine · 2022Review
- Cohesin mutations in myeloid malignancies.Blood · 2021Review
- Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.Scientific reports · 2021Article
- BETting on a Transcriptional Deficit as the Main Cause for Cornelia de Lange Syndrome.Frontiers in molecular biosciences · 2021Review
- Identification of HCC-Related Genes Based on Differential Partial Correlation Network.Frontiers in genetics · 2021Article
- MiR-187-3p Enhances Propranolol Sensitivity of Hemangioma Stem Cells.Cell structure and function · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPreviously, we reported that high expression of nipped-B-like protein (NIPBL) was strongly correlated with poor prognosis, tumor differentiation, and lymph node metastasis. Survival analysis indicated that NIPBL expression was a potential prognostic factor for non-small cell lung cancer (NSCLC). Moreover, loss of NIPBL decreased lung cancer cells proliferation, migration, invasion and promoted apoptosis as well as sensitivity to chemotherapeutic agents. However, the deep mechanisms were not explored. PURPOSE: The objective of this study was to identify the role of NIPBL in DNA damage response, as well as autophagy pathway, so as to interpret the mechanisms of how NIPBL knockdown enhances the chemosensitivity of lung cancer cell.
methodsCells (NCI-H1299 and NCI-H1650) were transfected by specific siRNAs before immunofluorescence and single-cell gel electrophoresis, which were mainly used to observe the differences of DNA damage in different groups. Additionally, protein were obtained and then analyzed by western blot and mass spectroscopy.
resultsIn this study, we found that knockdown of NIPBL resulted in accumulation of phosphorylated H2AX (γ-H2AX) foci and higher levels of DNA damage, as revealed by comet assay. Western blot assay revealed that loss of NIPBL decreased expression of ATM/ATR, Rad3-related protein and Ku70/Ku80, but increased expression of LC3-B and depletion of p62. Using mass spectroscopy, we identified eight proteins that were significantly differentially expressed upon NIPBL knockdown. Gene Ontology analysis revealed that these proteins are mainly involved in DNA repair, mismatch repair, and binding to damaged DNA. The expression changes in two of the proteins, MSH2 and STAT1, were verified by Western blotting in NIPBL-knockdown cells.
conclusionsIn summary, these results reflected that loss of NIPBL impairs the DNA damage response and promotes autophagy. And NIPBL suppression may represent a novel strategy for preventing chemotherapy resistance in lung cancer.
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