ArticleAmerican journal of translational research2021
CDKN2B-AS1 promotes the proliferation, clone formation, and invasion of nasopharyngeal carcinoma cells by regulating miR-98-5p/E2F2 axis.
Article in American journal of translational research, 2021. 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, 6 citations in OpenAlex.
- Downregulation of lncRNA CDKN2B-AS1 attenuates inflammatory response in mice with allergic rhinitis by regulating miR-98-5p/SOCS1 axis.Functional & integrative genomics · 2024Article
- High-throughput identification of regulatory elements and functional assays to uncover susceptibility genes for nasopharyngeal carcinoma.American journal of human genetics · 2023Article
- Long noncoding RNA CDKN2B-AS1 silencing protects against esophageal cancer cell invasion and migration by inactivating the TFAP2A/FSCN1 axis.The Kaohsiung journal of medical sciences · 2022Article
- Cuproptosis-related gene SLC31A1 is a potential predictor for diagnosis, prognosis and therapeutic response of breast cancer.American journal of cancer research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the effect of CDKN2B antisense RNA 1 (CDKN2B-AS1) on the proliferation, clone formation, and invasion of nasopharyngeal carcinoma (NPC) cells by regulating miR-98-5p/E2F transcription factor 2 (E2F2) axis.
methodsThe expressions of CDKN2B-AS1, miR-98-5p, and E2F2 in NPC tissues and cell lines (SUNE-1, 5-8F, 6-10B, and HK-1) as well as in peritumoral normal tissues and cell line NP69 were determined by qRT-PCR. Subcellular localization of CDKN2B-AS1 was detected using the fluorescence
resultsCDKN2B-AS1 was highly expressed in NPC tissues and cells, whereas the expression of miR-98-5p decreased in the NPC tissues and cells. Silencing of CDKN2B-AS1 inhibited the proliferation, clone formation, and invasion of NPC cells (all P<0.05). CDKN2B-AS1 acted asceRNA of miR-98-5p, and miR-98-5p inhibitor could partially reverse the inhibitory effect of silencing CDKN2B-AS1 on NPC cells (all P<0.05). CDKN2B-AS1 upregulated E2F2 by inhibiting miR-98-5p, and the upregulation of E2F2 partially reversed the inhibitory effect of miR-98-5p overexpression on the NPC cells (all P<0.05).
conclusionCDKN2B-AS1, as a lncRNA, can regulate E2F2 by sponging miR-98-5p to promote the proliferation, clone formation, and invasion of NPC cells.
Indexed as
Identifiers
35035684PMC8748104W4206871804What OpenQuestion holds
Registered trials
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.