ArticleCancer cell international2020
MIAT inhibits proliferation of cervical cancer cells through regulating miR-150-5p.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Clinicopathological and Prognostic Significance of Long Non-coding RNA MIAT in Human Cancers: A Review and Meta-Analysis.Frontiers in genetics · 2021Pooled it
- ETV6 Rearrangement Suppresses CDKN1B Transcription by Disrupting an Intragenic Super-enhancer in Acute Lymphoblastic Leukemia.Cancer research · 2026Article
- MIAT: A pivotal oncogenic long noncoding RNA tunning the hallmarks of solid malignancies.Translational oncology · 2025Article
- LncRNA-miRNA-mRNA regulatory axes as potential biomarkers in cervical cancer: a comprehensive overview.Molecular biology reports · 2025Review
- Prognosis Analysis and Validation of Fatty Acid Metabolism-Related lncRNAs and Tumor Immune Microenvironment in Cervical Cancer.Journal of immunology research · 2022Article
- CD105 expression is associated with invasive capacity in ovarian cancer and promotes invasiveness by inhibiting NDRG1 and regulating the epithelial-mesenchymal transition.American journal of translational research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo characterize the MIAT expression in cervical cancer and elucidate its mechanistic involvement in the tumor biology of this disease.
methodsThe relative expression of MIAT and miR-150 was determined by real-time PCR. Cell proliferation was measured by the CCK-8 and clonogenic assay. The anchorage-independent growth was evaluated by soft agar assay. The in vivo tumor progression was assayed with xenograft mice model. The regulatory effect of miR-150 on MIAT was interrogated by luciferase reporter assay. The endogenous CNKD1B protein was detected by western blotting.
resultsThe low expression of MIAT was characterized in cervical cancer, which associated with relatively poor prognosis. Ectopic expression of MIAT inhibited malignant growth of cervical cancer both in vitro and in vivo. Mechanistically, MIAT regulated CDKN1B expression via competition with miR-150, and miR-150-inhibition directly suppressed cervical cancer cell growth.
conclusionsOur study characterized the anti-tumor property of MIAT in cervical cancer and elucidated its competitively regulation of CDKN1B with miR-150. Our data highlighted the critical role of MIAT-miR-150-CDKN1B signaling axis in cervical cancer.
Indexed as
Identifiers
What 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.