ArticleBioengineered2022
LINC00472 suppresses oral squamous cell carcinoma growth by targeting miR-455-3p/ELF3 axis.
Article in Bioengineered, 2022. 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, 15 citations in OpenAlex.
- Overexpression of LINC00472 alleviates diabetic kidney disease progression via the miR-21-5p/STAT3 axis.Renal failure · 2026Article
- Article
- ELF3 Overexpression Contributes to the Malignant Transformation of HPV16 E6/E7-Immortalized Keratinocytes by Promoting CCNE2 Expression.Journal of microbiology and biotechnology · 2024Article
- Competing endogenous RNAs network dysregulation in oral cancer: a multifaceted perspective on crosstalk and competition.Cancer cell international · 2024Review
- RUNX1/miR-429 feedback loop promotes growth, metastasis, and epithelial-mesenchymal transition in oral squamous cell carcinoma by targeting ITGB1.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Novel genome-wide DNA methylation profiling reveals distinct epigenetic landscape, prognostic model and cellular composition of early-stage lung adenocarcinoma.Journal of translational medicine · 2024Article
- LINC00847 drives pancreatic cancer progression by targeting the miR-455-3p/HDAC4 axis.Archives of medical science : AMS · 2024Article
- Luteolin impacts deoxyribonucleic acid repair by modulating the mitogen-activated protein kinase pathway in colorectal cancer.Bioengineered · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LINC00472 is reported to play a role in suppressing tumors in cancers such as lung cancer and hepatocellular carcinoma, among others. We made investigations into the effects of LINC00472 in oral squamous cell carcinoma (OSCC) progression to explore the underlying molecular mechanisms. By qRT-PCR, we assessed the LINC00472 expression in OSCC tissues and cells and performed functional analysis to investigate how LINC00472/miR-455-3p/ELF3 impacts OSCC cell proliferation, apoptosis, and cell cycle. The role that LINC00472 plays in OSCC tumor growth was examined by establishing a xenograft model. Down-regulation of LINC00472 occurred in tissues and cells of an OSCC tumor. LINC00472 overexpression caused OSCC cell proliferation to be inhibited, cell apoptosis to be promoted, and cell cycle arrest to be induced. As a competing endogenous RNA (ceRNA), LINC00472 can block miR-455-3p function and further promote ELF3 expression. The overexpression of miR-455-3p or ELF3 knockdown was shown to be capable of reversing the anti-tumor effects of LINC00472 in OSCC. In vivo experiments confirmed the tumor-suppressing role of LINC00472 in the progression of OSCC. In short, we found that the novel LINC00472 inhibits OSCC growth via the miR-455-3p/ELF3 axis. LINC00472 and its targeted miR-455-3p/ELF3 axis may represent valuable targets for treating OSCC.
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