Evidence map›Paper›PMID 32767499›Full record

ArticleThoracic cancer2020

Circular RNA CirCHIPK3 promotes cell proliferation and invasion of breast cancer by sponging miR-193a/HMGB1/PI3K/AKT axis.

Zhen-Gang Chen, Hong-Jie Zhao, Ling Lin, Jin-Bo Liu, Jing-Zhen Bai, Guang-Shun Wang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

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  12. Mechanisms of apoptosis-related non-coding RNAs in ovarian cancer: a narrative review.Apoptosis : an international journal on programmed cell death · 2025
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  16. Circular RNAs and Cancers.Advances in experimental medicine and biology · 2025
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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

6 authors at 2 institutions in 1 country.

Zhen-Gang ChenDeapartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Hong-Jie ZhaoDeapartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Ling LinDeapartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Jin-Bo LiuDeapartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Jing-Zhen BaiDeapartment of General Surgery, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.
Guang-Shun WangDeapartment of Oncology, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin, China.ORCID 0000-0003-2769-3460
Tianjin Medical University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aim of this study was to explore the potential mechanism of circular RNA (circRNA) CirCHIPK3 on the malignant proliferation and metastasis of breast cancer (BC).

methodsHuman BC samples and their matched normal adjacent tissues were obtained from 50 patients to assess the expression of CirCHIPK3 and its relationship with BC prognosis. A series of in vitro and in vivo functional experiments were carried out to elucidate the role of CirCHIPK3 in BC progression and its underlying molecular mechanisms. Moreover, the interaction of CirCHIPK3, miR-193a, and HMGB1 was examined using bioinformatics, FISH, RIP, RNA-pull down and luciferase reporter assays. Western blot analysis was performed to examine the expression of HMGB1, p-PI3K, total PI3K, p-AKT, and AKT after si-CirCHIPK3 transfection.

resultsUpregulation of CirCHIPK3 was identified in BC, which predicted a worse prognosis in BC patients. Furthermore, it was found that CirCHIPK3 facilitated cell proliferation, migration, and invasion in BC by regulating miR-193a/HMGB1/PI3K/AKT signaling. CirCHIPK3 acted as a sponge for miR-193a to facilitate HMGB1 expression. si-CirCHIPK3 also inhibited tumor growth of BC in nude mice. si-CircCHIPK3 decreased HMGB1/PI3K/AKT signal expression in MDA-MB-231 cells, whereas overexpression of CircCHIPK3 enhanced HMGB1/PI3K/AKT signal.

conclusionsCirCHIPK3 regulated miR-193a/HMGB1/PI3K/AKT signaling to facilitate BC development and progression, providing a novel therapeutic target for BC.

Indexed as

AnimalsBreast NeoplasmsCell ProliferationFemaleHumansMiceMice, NudeMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, CircularTransfectionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, CircularBreast cancerCirCHIPK3endogenous competitive RNAhigh-mobility group box-1miR-193a

Identifiers

PMID32767499
PMCPMC7471055
OpenAlexW3048099007

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.