ArticleOncology letters2016
miRNA-335 and miRNA-182 affect the occurrence of tongue squamous cell carcinoma by targeting survivin.
Article in Oncology letters, 2016. 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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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Current status of traditional Chinese medicine in modulating mitochondrial metabolic abnormalities in tumors.Cancer biology & medicine · 2025Review
- LINC00511 Knockdown Suppresses Resistance to Cisplatin in Lung Adenocarcinoma by Interacting with miR-182-3p and BIRC5.Molecular biotechnology · 2022Article
- Article
- MicroRNA-182 downregulates Wnt/β-catenin signaling, inhibits proliferation, and promotes apoptosis in human osteosarcoma cells by targeting HOXA9.Oncotarget · 2017Article
Corrections and comments
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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
The aim of the present study was to characterize the roles of two microRNAs (miRs) that have been reported to be differentially expressed in tongue squamous cell carcinoma (TSCC), miR-335 and miR-182. In total, 20 tumor tissue samples and 20 corresponding adjacent non-cancerous samples were collected from patients with TSCC to measure the expression of miR-335 and miR-182 and the potential shared target of these miRs, survivin, using reverse transcription-quantitative polymerase chain reaction and western blotting. In the TSCC tissue samples, significantly decreased expression of the two miRs and increased expression of survivin were detected compared with adjacent non-cancerous controls. Subsequently, it was confirmed that survivin was the target gene of miR-335 and miR-182 using a luciferase assay in TSCC cells. In order to examine the function of miR-335 and miR-182 in the development of TSCC, TSCC cells were transiently transfected with the mimics of the two miRs, and it was confirmed that the introduction of miR-335 and miR-182 to cells suppressed the expression of survivin and markedly inhibited the proliferation of the TSCC cells. Furthermore, miR-335 and miR-182 were found to induce cell cycle arrest by suppressing the expression of survivin. The present study revealed a negative regulatory role of miR-335 and miR-182 in the proliferation of TSCC cells by targeting survivin, and miR-335 and miR-182 may be novel therapeutic targets for the treatment of TSCC.
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