ArticleTranslational cancer research2020
Chromodomain-helicase-DNA-binding protein 1-like (CHD1L) silencing inhibits gastric cancer cell proliferation, invasion, and migration.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Disrupted transcriptional networks regulated by CHD1L during neurodevelopment underlie the mirrored neuroanatomical and growth phenotypes of the 1q21.1 copy number variant.Nucleic acids research · 2025Article
- CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- Interference with CHD1L inhibits the malignant progression and enhances cisplatin sensitivity of ovarian cancer cells by binding PLK1.Journal of ovarian research · 2025Article
- miR-193b-3p and miR-346 Exert Antihypertensive Effects in the Rostral Ventrolateral Medulla.Journal of the American Heart Association · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe aimed to investigate the effect of chromodomain-helicase-DNA-binding protein 1-like (CHD1L) silencing on the biological behavior of gastric cancer cells.
methodsSmall hairpin RNA (shRNAs) targeting CHD1L were designed and transduced into BGC-823 human gastric cancer cells. Expression of p53, p21, nerve growth factor IB (Nur77), and ARHGEF9 was assessed by western blotting, and the effect of CHD1L silencing on gastric cancer cell proliferation, apoptosis, and migration was examined by MTT, flow cytometry, and wound healing assays, respectively.
resultsIn CHD1L-shRNA-1-treated cells, the expression of p53, p21, Nur77, and ARHGEF9 was significantly upregulated, and the number of apoptotic cells was significantly increased compared to the shRNA-negative control (NC; P<0.05). Additionally, the number of cells in the G1 phase was significantly increased among CHD1L-shRNA-1-treated cells. In contrast, the number of cells in the S phase was significantly decreased among CHD1L-shRNA-1-treated cells compared to shRNA-NC-treated cells (P<0.05). Following CHD1L silencing, there were 58.63±10.97 invading cells compared to 144.95±12.68 and 148.49±17.86 in the shRNA-NC and untreated groups, respectively (P<0.05). After 24 h, CHD1L-silenced BGC-823 cells migrated 0.54±0.34 µm compared to 1.34±0.26 and 1.31±0.31 µm in the shRNA-NC and untreated groups, respectively (P<0.05).
conclusionsCHD1L silencing significantly inhibited the proliferation, invasion, and migration of BGC-823 gastric cancer cells and induced apoptosis. Knockdown of CHD1L may present a novel approach for treating gastric cancer.
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