Evidence map›Paper›PMID 31166382›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2019

Downregulation of lncRNA CCDC26 contributes to imatinib resistance in human gastrointestinal stromal tumors through IGF-1R upregulation.

Jingyi Yan, Didi Chen, Xiaolei Chen, Xuecheng Sun, Qiantong Dong, Changyuan Hu, Feng Zhou, Wei Chen

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

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  11. Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022
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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

8 authors at 2 institutions in 1 country.

Jingyi YanDepartment of Gastroenterology and General Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Didi ChenDepartment of Radiotherapy and Medical Oncology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Xiaolei ChenDepartment of Gastroenterology and General Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Xuecheng SunDepartment of Gastroenterology and Hepatology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Qiantong DongDepartment of Gastroenterology and General Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Changyuan HuDepartment of Gastroenterology and General Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Feng ZhouDepartment of Gastroenterology and General Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Wei ChenTongde Hospital of Zhejiang Province, Hangzhou, Zhejiang Province, China.
Wenzhou Medical University · CNTongde Hospital of Zhejiang Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imatinib is the first line of therapy for patients with metastatic or gastrointestinal stromal tumors (GIST). However, drug resistance limits the long-term effect of imatinib. Long non-coding RNAs (lncRNAs) are emerging as key players in regulating drug resistance in cancer. In this study, we investigated the association between lncRNA CCDC26 and IGF-1R in GIST and their involvement in drug resistance. Considering the key role of lncRNAs in drug resistance in cancer, we hypothesized that IGF-1R is regulated by lncRNAs. The expression of a series of reported drug resistance-related lncRNAs, including CCDC26, ARF, H19, NBR2, NEAT1, and HOTAIR, in GIST cells treated with imatinib H19 was examined at various time-points by qRT-PCR. Based on our results and published literature, CCDC26, a strongly down-regulated lncRNA following imatinib treatment, was chosen as our research target. GIST cells with high expression of CCDC26 were sensitive to imatinib treatment while knockdown of CCDC26 significantly increased the resistance to imatinib. Furthermore, we found that CCDC26 interacted with c-KIT by RNA pull down, and that CCDC26 knockdown up-regulated the expression of IGF-1R. Moreover, IGF-1R inhibition reversed CCDC26 knockdown-mediated imatinib resistance in GIST. These results indicated that treatments targeting CCDC26-IGF-1R axis would be useful in increasing sensitivity to imatinib in GIST.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisCell Line, TumorDown-RegulationFlow CytometryGene Expression Regulation, NeoplasticHumansImatinib MesylateIntracellular Signaling Peptides and ProteinsReceptor, IGF Type 1Receptors, SomatomedinRNA, Long NoncodingSignal TransductionAntineoplastic AgentsIGF1R protein, humanImatinib MesylateIntracellular Signaling Peptides and Proteinslong noncoding RNA CCDC26, humanReceptor, IGF Type 1Receptors, SomatomedinRNA, Long Noncoding

Identifiers

PMID31166382
PMCPMC6556970
OpenAlexW2947215741

What OpenQuestion holds

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LicenceCC BY
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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.