Evidence map›Paper›PMID 28219405›Full record

ArticleJournal of hematology & oncology2017

TTBK2 circular RNA promotes glioma malignancy by regulating miR-217/HNF1β/Derlin-1 pathway.

Jian Zheng, Xiaobai Liu, Yixue Xue, Wei Gong, Jun Ma, Zhuo Xi, Zhongyou Que, Yunhui Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed
14.1field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 229 citations in OpenAlex.

  1. Article
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  5. Circular RNAs in Brain Physiology and Neurologic Diseases.Advances in experimental medicine and biology · 2025
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69 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Jian ZhengDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Xiaobai LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Yixue XueDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, 110122, People's Republic of China.
Wei GongDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, 110122, People's Republic of China.
Jun MaDepartment of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, 110122, People's Republic of China.
Zhuo XiDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Zhongyou QueDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China.
Yunhui LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, 110004, People's Republic of China. liuyh_cmuns@163.com.
China Medical University · CNShenyang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCircular RNAs are a subgroup of non-coding RNAs and generated by a mammalian genome. Herein, the expression and function of circular RNA circ-TTBK2 were investigated in human glioma cells.

methodsFluorescence in situ hybridization and quantitative real-time PCR were conducted to profile the cell distribution and expression of circ-TTBK2 and microRNA-217 (miR-217) in glioma tissues and cells. Immunohistochemical and western blot were used to determine the expression of HNF1β and Derlin-1 in glioma tissues and cells. Stable knockdown of circ-TTBK2 or overexpression of miR-217 glioma cell lines (U87 and U251) were established to explore the function of circ-TTBK2 and miR-217 in glioma cells. Further, luciferase reports and RNA immunoprecipitation were used to investigate the correlation between circ-TTBK2 and miR-217. Cell Counting Kit-8, transwell assays, and flow cytometry were used to investigate circ-TTBK2 and miR-217 function including cell proliferation, migration and invasion, and apoptosis, respectively. ChIP assays were used to ascertain the correlations between HNF1β and Derlin-1.

resultsWe found that circ-TTBK2 was upregulated in glioma tissues and cell lines, while linear TTBK2 was not dysregulated in glioma tissues and cells. Enhanced expression of circ-TTBK2 promoted cell proliferation, migration, and invasion, while inhibited apoptosis. MiR-217 was downregulated in glioma tissues and cell lines. We also found that circ-TTBK2, but not linear TTBK2, acted as miR-217 sponge in a sequence-specific manner. In addition, upregulated circ-TTBK2 decreased miR-217 expression and there was a reciprocal negative feedback between them in an Argonaute2-dependent manner. Moreover, reintroduction of miR-217 significantly reversed circ-TTBK2-mediated promotion of glioma progression. HNF1β was a direct target of miR-217, and played oncogenic role in glioma cells. Remarkably, circ-TTBK2 knockdown combined with miR-217 overexpression led to tumor regression in vivo.

conclusionsThese results demonstrated a novel role circ-TTBK2 in the glioma progression.

Indexed as

ApoptosisBiopsyCell Line, TumorCell MovementCell ProliferationDisease ProgressionGliomaHepatocyte Nuclear Factor 1-betaHumansMembrane ProteinsMicroRNAsNeoplasm InvasivenessProtein Serine-Threonine KinasesRNARNA, CircularSignal TransductionDERL1 protein, humanHepatocyte Nuclear Factor 1-betaHNF1B protein, humanMembrane ProteinsMicroRNAsMIRN217 microRNA, humanProtein Serine-Threonine KinasesRNARNA, Circulartau-tubulin kinasecirc-TTBK2Circular RNAsGliomaMicroRNAsmiR-217

Identifiers

PMID28219405
PMCPMC5319142
OpenAlexW2591096977

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Registered trials

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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.