Evidence map›Paper›PMID 32181582›Full record

ArticleJournal of cellular and molecular medicine2020

MiR-3116 sensitizes glioma cells to temozolomide by targeting FGFR1 and regulating the FGFR1/PI3K/AKT pathway.

Shiqi Kong, Yingxiao Cao, Xin Li, Zhenzhong Li, Yuling Xin, Yan Meng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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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.

Shiqi KongDepartment of Neurosurgery, Xingtai People's Hospital, Xingtai, China.
Yingxiao CaoDepartment of Neurosurgery, Xingtai People's Hospital, Xingtai, China.ORCID 0000-0002-2646-7608
Xin LiDepartment of Neurosurgery, The First People's Hospital of Shenyang, Shenyang, China.
Zhenzhong LiDepartment of Neurosurgery, Xingtai People's Hospital, Xingtai, China.ORCID 0000-0003-0033-6682
Yuling XinDepartment of Neurosurgery, Xingtai People's Hospital, Xingtai, China.
Yan MengDepartment of Operating Room, Xingtai People's Hospital, Xingtai, China.
Hebei Medical University · CNShenyang First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioma is a brain tumour that is often diagnosed, and temozolomide (TMZ) is a common chemotherapeutic drug used in glioma. Yet, resistance to TMZ is a chief hurdle towards curing the malignancy. The current work explores the pathways and involvement of miR-3116 in the TMZ resistance. miR-3116 and FGFR1 mRNA were quantified by real-time PCR in malignant samples and cell lines. Appropriate assays were designed for apoptosis, viability, the ability to form colonies and reporter assays to study the effects of the miR-3116 or FGFR1. The involvement of PI3K/AKT signalling was assessed using Western blotting. Tumorigenesis was evaluated in an appropriate xenograft mouse model in vivo. This work revealed that the levels of miR-3116 dipped in samples resistant to TMZ, while increased miR-3116 caused an inhibition of the tumour features mentioned above to hence augment TMZ sensitivity. miR-3116 was found to target FGFR1. When FGFR1 was overexpressed, resistance to TMZ was augmented and reversed the sensitivity caused by miR-3116. Our findings further confirmed PI3K/AKT signalling pathway is involved in this action. In conclusion, miR-3116 sensitizes glioma cells to TMZ through FGFR1 downregulation and the PI3K/AKT pathway inactivation. Our results provide a strategy to overcome TMZ resistance in glioma treatment.

Indexed as

AnimalsApoptosisCarcinogenesisCell Line, TumorCell ProliferationDacarbazineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGliomaHumansMiceMicroRNAsOncogene Protein v-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1DacarbazineFGFR1 protein, humanMicroRNAsOncogene Protein v-aktPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1Temozolomidedrug resistanceFGFR1FGFR1/PI3K/AKTmiR-3116temozolomide

Identifiers

PMID32181582
PMCPMC7176860
OpenAlexW3011062361

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.