ArticleOncology letters2020
Effects of CDK6 regulated by miR-298 on proliferation and apoptosis of thyroid cancer cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Harnessing extracellular vesicle-mediated crosstalk between T cells and cancer cells for therapeutic applications.Journal of controlled release : official journal of the Controlled Release Society · 2025Review
- Tumor-derived exosome PPP3CB induce gemcitabine resistance by regulating miR-298/STAT3 in pancreatic cancer.Heliyon · 2024Article
- YTHDC1 aggravates high glucose-induced retinal vascular endothelial cell injury via m6A modification of CDK6.Biology direct · 2024Article
- Introducing Circulating Vasculature-Related Transcripts as Biomarkers in Coronary Artery Disease.Molecular diagnosis & therapy · 2023Article
- MiR-20b Tissue Expression Level Displays the Diagnostic Value in Papillary Thyroid Carcinoma.Medical journal of the Islamic Republic of Iran · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effects of CDK6 regulated by miR-298 on proliferation and apoptosis of thyroid cancer cells were explored. Seventy-five cases of thyroid carcinoma and adjacent tissues were collected. The expression levels of miR-298 and CDK6 mRNA in tissues and cells were detected by RT-PCR. In addition, thyroid cancer cells and human normal thyroid cells Nthy-ori3-1 were purchased, with the former transfected with miR-298-mimics, miR-298-inhibitor, miR-NC, si-CDK6, si-NC, Sh-CDK6, Sh-NC to build cell models. Then the expression levels of miR-298 and CDK6 in thyroid cancer tissues and cells were detected by qRT-PCR, and the expression of CDK6, Bax, Bcl-2 and caspase-3 by WB. CCK-8 and flow cytometry were employed to detect cell proliferation and apoptosis, and dual luciferase report was adopted to determine the relationship between miR-298 and CDK6. miR-298 was underexpressed in thyroid cancer, and CDK6 was highly expressed in thyroid cancer. Cell experiments revealed that overexpression of miR-298 or inhibition of CDK6 expression could suppress cell proliferation, promote apoptosis, and significantly increase the expression levels of Bax and caspase-3 proteins, decrease Bcl-2 protein expression, which was contrary to the biological phenotype of cells after inhibition of miR-298 or further overexpression of CDK6. Dual luciferase report confirmed that miR-298 was a targeting site of CDK6. miR-298 can inhibit the proliferation of thyroid cells and promote apoptosis of thyroid cancer cells by regulating the expression of CDK6, which is expected to be a potential target for clinical application.
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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.