ArticleMolecular biotechnology2024
LncRNA ZNF667-AS1 Targets miR-523-3p/KIF5C Axis to Hinder Colon Cancer Progression.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Leveraging Kinesin Family as Key Regulators of Malignant Progression and the Immunometabolic Niche for Precision Oncology.Technology in cancer research & treatmentReview
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LncRNA ZNF667-AS1 plays an important role in the carcinogenesis and progression of various cancers. However, their role in colon cancer (CC) remains unclear. The expression of ZNF667-AS1, KIF5C, and miR-523-3p in CC cells and tissues was analyzed using RT-qPCR and western blotting. CCK-8 scratch-wound assay, western blotting, and flow cytometry were conducted to investigate the malignant activity of CC in vitro. Luciferase reporter, RNA pull-down, and Ago2 immunoprecipitation (RIP) experiments were conducted to ascertain the association of miR-523-3p with ZNF667-AS1 and KIF5C 3'UTR. Xenograft tumor experiments were also performed. CC cells and tissues showed low expression of NF667-AS1 and KIF5C and elevated expression of miR-523-3p. ZNF667-AS1 overexpression attenuates proliferation and migration of CC cells, restores inactivated apoptosis in vitro, and inhibits tumor growth in vivo. MiR-523-3p targets both ZNF667-AS1 and the KIF5C 3'UTR. ZNF667-AS1 overexpression in SW480 and SW620 cells attenuated the oncogenic effect of miR-523-3p in CC. However, this attenuating effect was counteracted by KIF5C overexpression. ZNF667-AS1 sequestered miR-523-3, reducing miR-523-3p-mediated inhibition of KIF5C expression, thereby repressing colon carcinogenesis in vitro. Our findings shed light on a novel anticancer strategy that could potentially combat CC.
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Registered trials
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