Evidence map›Paper›PMID 30987661›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2.

Hongtao Zhu, Xiaoling Gan, Xingwei Jiang, Shuai Diao, Huan Wu, Jianguo Hu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
17.1field-weighted citation impact, top 1% 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

158 citing papers in PubMed, 1 synthesis or guideline pooled it, 290 citations in OpenAlex.

  1. Emerging Roles of mFrontiers in oncology · 2022
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98 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Hongtao ZhuDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China.
Xiaoling GanDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China.
Xingwei JiangDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China.
Shuai DiaoDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China.
Huan WuDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China.
Jianguo HuDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China. angeljianguo@163.com.
Dalian Medical University · CNChongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundALKBH5 regulated the malignant behavior of breast cancer and glioblastoma. However, the expression and function of ALKBH5 in epithelial ovarian cancer have not yet been determined. In the present study, we investigated the expression and function of ALKBH5 in epithelial ovarian cancer with respect to its potential role in the tumorigenesis of the disease as well as an early diagnostic marker.

methodsImmunohistochemistry and western blot were used to detect protein expression. Gene silencing and over-expression experiment were used to study gene function. Cell proliferation assay and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The nude mouse tumor formation experiment was used to evaluate the growth of cells in vivo.

resultsThe expression of ALKBH5 was found to be increased in epithelial ovarian cancer tissue as compared to the normal ovarian tissues. The silencing of ALKBH5 in SKOV3 cells enhanced the autophagy and inhibited the proliferation and invasion in vitro and in vivo, whereas the ectopic expression of ALKBH5 in A2780 cells exerted an opposite effect. Mechanical study revealed that ALKBH5 physically interacted with HuR. ALKBH5 activated EGFR-PIK3CA-AKT-mTOR signaling pathway. Also, ALKBH5 enhanced the stability of BCL-2 mRNA and promoted the interaction between Bcl-2 and Beclin1.

conclusionOverall, the present study identified ALKBH5 as a candidate oncogene in epithelial ovarian cancer and a potential target for ovarian cancer therapy.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAlkB Homolog 5, RNA DemethylaseAnimalsAutophagyBeclin-1Carcinoma, Ovarian EpithelialCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDNA MethylationErbB ReceptorsFemaleHeterograftsALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseBeclin-1EGFR protein, humanErbB ReceptorsMicroRNAsMIRN7-1 microRNA, humanProto-Oncogene Proteins c-bcl-2ALKBH5AutophagyBCL-2Beclin1miR-7, EGFR

Identifiers

PMID30987661
PMCPMC6463658
OpenAlexW2945580636

What OpenQuestion holds

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LicenceCC BY
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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.