ArticleOncology reports2020
miR‑1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Mechanistic insights into the lncRNA-Notch signaling axis in tumors.Frontiers in cell and developmental biology · 2026Review
- Signaling networks and MiRNA crosstalk in ovarian cancer chemoresistance.Journal of ovarian research · 2025Review
- Article
- Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications.Cancers · 2025Review
- Copy number variation analysis identifies MIR9-3 and MIR1299 as novel miRNA candidate genes for CAKUT.Pediatric nephrology (Berlin, Germany) · 2024Article
- LncRNAIranian journal of public health · 2022Article
- Long non-coding RNA (LncRNA) CHROMR promotes the expression of theTranslational cancer research · 2022Article
- Circ_0001955 plays a carcinogenic role in breast cancer via positively regulating GLUT1 via decoying miR-1299.Thoracic cancer · 2022Article
- Long non-coding MELTF Antisense RNA 1 promotes and prognosis the progression of non-small cell lung cancer by targeting miR-1299.Bioengineered · 2022Article
- LncRNAFrontiers in medicine · 2022Article
- The expression of ASAP3 and NOTCH3 and the clinicopathological characteristics of adult glioma patients.Open medicine (Warsaw, Poland) · 2022Article
- Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1.Molecular medicine reports · 2021Article
- Role of long noncoding RNA taurine-upregulated gene 1 in cancers.Molecular medicine (Cambridge, Mass.) · 2021Review
- Non-Coding RNAs as Biomarkers of Tumor Progression and Metastatic Spread in Epithelial Ovarian Cancer.Cancers · 2021Review
- The role and underlying mechanism of miR-1299 in cancer.Future science OA · 2021Review
- The Role of Notch3 Signaling in Cancer Stemness and Chemoresistance: Molecular Mechanisms and Targeting Strategies.Frontiers in molecular biosciences · 2021Review
- LncRNAs in Ovarian Cancer Progression, Metastasis, and Main Pathways: ceRNA and Alternative Mechanisms.International journal of molecular sciences · 2020Review
- LncRNA TUG1 contributes to the tumorigenesis of lung adenocarcinoma by regulating miR-138-5p-HIF1A axis.International journal of immunopathology and pharmacologyArticle
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed the oncogenic role of notch reporter 3 (NOTCH3) in ovarian cancer (OC). However, the possible regulators and mechanisms underlying notch receptor 3 (NOTCH3)‑mediated behaviors in OC remain to be completely investigated. In the present study, we aimed to identify regulators of NOTCH3 and their interactions underlying the pathogenesis of OC. Bioinformatics analysis and luciferase reporter assay were used to identify potential regulatory miRNAs and lncRNAs of NOTCH3 in OC. Several in vivo and in vitro assays were performed to evaluate their effects on the proliferative ability mediated by NOTCH3. We identified microRNA‑1299 (miR‑1299) as a novel negative regulator of NOTCH3. miR‑1299 was downregulated in OC and was found to be considerably correlated with tumor differentiation. Upregulation of miR‑1299 inhibited cell proliferation, colony formation, and 5‑ethynyl‑2'‑deoxyuridine (EdU) incorporation, as well as induced cell cycle arrest in the G0G1 phase in OC cells. Overexpression of miR‑1299 in xenograft mouse models suppressed tumor growth in vivo. The lncRNA taurine upregulated gene 1 (TUG1), acting as a sponge of miR‑1299, was found to upregulate NOTCH3 expression and promote cell proliferation in OC through the competing endogenous RNA mechanism. In addition, TUG1 was found to be a potential downstream target of NOTCH3, forming a miR‑1299/NOTCH3/TUG1 feedback loop in the development of OC. Collectively, our findings improve the understanding of NOTCH3‑mediated regulation in OC pathogenesis and facilitate the development of miRNA‑ and lncRNA‑directed diagnostics and therapeutics against this disease.
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.