Evidence map›Paper›PMID 28086946›Full record

ArticleJournal of ovarian research2017

MiR-1307 promotes ovarian cancer cell chemoresistance by targeting the ING5 expression.

Wen-Ting Chen, Yu-Jia Yang, Zhen-Dong Zhang, Qiang An, Na Li, Wei Liu, Bing Yang

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 79 citations in OpenAlex.

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  10. The roles of ING5 in cancer: A tumor suppressor.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

7 authors at 1 institution in 1 country.

Wen-Ting ChenAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Yu-Jia YangAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Zhen-Dong ZhangAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Qiang AnAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Na LiAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Wei LiuAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China.
Bing YangAffiliated hospital of Zunyi Medical College, Zunyi, Guizhou, 563000, People's Republic of China. bingyang810@163.com.
Affiliated Hospital of Zunyi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe aimed to investigate the function of miR-1307 in chemoresistance and to explore its chemoresistance mechanism in ovarian cancer.

methodsIC50 determination was used to test the chemoresistance profling in ovarian cancer cells. QRT-PCR or western blot was used to validate the expression level of miR-1307 and candidate gene or protein. Colony formation assay and FITC-labeled enhanced Annexin V immunofluorescence were used to compare cell proliferation and apoptosis ability, respectively. The potential target gene and its biological function of miRNA-1307 were also analyzed. Bioinformatics and Luciferase Reporter Gene Assay were conducted to validate the regulation of miRNA-1307 on the ING5 expression. Xenografts assay was used to demonstrate the inhibiting effect of miR-1307 ASO and Taxol therapy against ovarian cancer in vivo.

resultsMiR-1307 was over-expressed in chemoresistant ovarian cancer cell line A2780/Taxol, and over-expression or loss of miR-1307 promoted or inhabited chemoresistance. And we also found that the over-expression of miR-1307 promoted proliferation and inhibited apoptosis in ovarian cancer cells. Besides, we demonstrated that ING5 was a direct target of miR-1307 and miR-1307 down-regulated the ING5 expression in ovarian cancer cells. Additionally, we showed that ING5 inhibited cell proliferation, promoted cell apoptosis and inhabited chemoresistance reversely. Furthermore, the up-regulated ability of cell apoptosis and down-regulated ability of chemoresistance following the loss of miR-1307 was reversed by adding ING5 siRNA in vitro. Finally, we proved the inhibiting effect of miR-1307 ASO and Taxol therapy by increasing the ING5 expression against ovarian cancer through xenografts assay in vivo.

conclusionOur results suggested that miR-1307 could promote ovarian cancer chemoresistance by targeting the ING5 expression and miR-1307 might serve as a therapeutic target for ovarian cancer.

Indexed as

Gene Expression Regulation, NeoplasticRNA Interference3' Untranslated RegionsAnimalsAntineoplastic AgentsAntineoplastic Agents, PhytogenicApoptosisBinding SitesCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalDrug Resistance, NeoplasmFemaleGene ExpressionHumans3' Untranslated RegionsAntineoplastic AgentsAntineoplastic Agents, PhytogenicING5 protein, humanMicroRNAsMIRN1307 microRNA, humanPaclitaxelTranscription FactorsTumor Suppressor ProteinsCell chemoresistanceING5miR-1307Ovarian cancer

Identifiers

PMID28086946
PMCPMC5234104
OpenAlexW2579768348

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.