Evidence map›Paper›PMID 37277864›Full record

ArticleThoracic cancer2023

Circ_0010235 confers cisplatin resistance in lung cancer by upregulating E2F7 through absorbing miR-379-5p.

Lifei Wang, Dongchang Wang, Zhen Xu, Yali Qiu, Gang Chen, Furong Tan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  4. miR-379-5p Inhibited the Proliferation of Acute Myeloid Leukemia Cells Through Negative Regulation ofTurkish journal of haematology : official journal of Turkish Society of Haematology · 2025
    Article
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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.

Lifei WangDepartment of Pulmonary and Critical Care Medicine, Changzhou Third People's Hospital, Changzhou, China.
Dongchang WangDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, China.
Zhen XuDepartment of Pulmonary and Critical Care Medicine, Changzhou Third People's Hospital, Changzhou, China.
Yali QiuDepartment of Pulmonary and Critical Care Medicine, Changzhou Third People's Hospital, Changzhou, China.
Gang ChenDepartment of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Hebei Medical University, Shijiazhuang, China.
Furong TanDepartment of Pulmonary and Critical Care Medicine, Changzhou Third People's Hospital, Changzhou, China.ORCID 0009-0000-7597-3729
Changzhou Third People's Hospital · CNHebei Medical University · CN

Funding

Changzhou Health and Green Seedling Talent Training Project 2059999Science and Technology Project of Changzhou Health Commission WZ201909
6 · The paper itself

Abstract

backgroundCisplatin (DDP) treatment is one of the most predominant chemotherapeutic strategies for lung cancer patients. Circular RNAs (circRNAs) have been revealed to participate in the chemoresistance in lung cancer. Hence, the role and mechanism of circ_0010235 in cisplatin resistance in lung cancer was investigated.

methodsExpression levels of circ_0010235, microRNA (miR)-379-5p and E2F transcription factor 7 (E2F7) were analyzed using quantitative reverse transcription PCR (qRT-PCR) and western blot. Cell DDP sensitivity, proliferation, apoptosis, invasion, and migration were detected by cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine (EDU) assay, flow cytometry and western blot, respectively. The binding interaction was verified using dual-luciferase reporter assay. A murine xenograft model was established to investigate effects in vivo.

resultsCirc_0010235 was highly expressed in DDP-resistant lung cancer tissues and cells. Knockdown of circ_0010235 elevated DDP sensitivity, constrained proliferation, invasion and migration as well as fostered apoptosis in DDP-resistant lung cancer cells. Moreover, circ_0010235 silencing boosted DDP sensitivity and impeded tumor growth in lung cancer in vivo. Mechanistically, circ_0010235 acted as a sponge for miR-379-5p to elevate the expression of its target E2F7. Rescue experiments showed that miR-379-5p inhibition attenuated circ_0010235 knockdown-evoked reduction on DDP resistance of DDP-resistant cancer cells. In addition, miR-379-5p re-expression elevated DDP sensitivity and suppressed the malignant phenotype of DDP-resistant lung cancer cells through miR-379-5p.

conclusionCirc_0010235 knockdown reduced DDP resistance and tumor growth via miR-379-5p/ E2F7 axis in lung cancer, suggesting an effective therapeutic target for lung cancer patients.

Indexed as

Lung NeoplasmsMicroRNAsRNA, CircularAnimalsApoptosisCell CountCell ProliferationCisplatinDrug Resistance, NeoplasmE2F7 Transcription FactorHumansMiceCisplatinE2F7 protein, humanE2F7 Transcription FactorMicroRNAsMIRN379 microRNA, humanRNA, Circularcirc_0010235cisplatin resistanceE2F7lung cancermiR-379-5p

Identifiers

PMID37277864
PMCPMC10344743
OpenAlexW4379508995

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.