Evidence map›Paper›PMID 32139670›Full record

ArticleCell death & disease2020

Silencing of circRACGAP1 sensitizes gastric cancer cells to apatinib via modulating autophagy by targeting miR-3657 and ATG7.

Ling Ma, Zhangding Wang, Mengyan Xie, Yunlin Quan, Weiyou Zhu, Fengming Yang, Chenhui Zhao, Yu Fan, Na Fang, Huning Jiang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 68 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

15 authors at 5 institutions in 1 country.

Ling Ma *Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Zhangding Wang *Department of Gastroenterology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu Province, China.
Mengyan Xie *Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Yunlin Quan *School of Mechanical Engineering, Jiangsu Key Laboratory for Design and Manufacture of Micro-Nano Biomedical Instruments, Southeast University, Nanjing, 211189, China.
Weiyou ZhuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Fengming YangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Chenhui ZhaoDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Yu FanCancer Institute, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, 212002, China.
Na FangCancer Institute, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, 212002, China.
Huning JiangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Qiang WangDepartment of Molecular Cell Biology and Toxicology, Cancer Center, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Shouyu WangDepartment of Molecular Cell Biology and Toxicology, Cancer Center, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Jianwei ZhouDepartment of Molecular Cell Biology and Toxicology, Cancer Center, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.
Xiaofeng ChenDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. xiaofengch198019@126.com.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. shuyongqian@njmu.edu.cn.
Nanjing Medical University · CNJiangsu Province Hospital · CNAffiliated Hospital of Jiangsu University · CNNanjing Drum Tower Hospital · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The positive results of the apatinib phase III trial have cast new light on treatment for patients with advanced gastric cancer (GC). However, in terms of safety, apatinib toxicities may lead to a dose modification or treatment interruption. Therefore, proper intervention is urgently needed to help patients benefit from apatinib treatment. In this study, we found that apatinib promoted autophagy activation via upregulation of ATG7 expression and autophagy inhibition enhanced apatinib-induced apoptosis. With microRNA and circular RNA-sequencing analyses of GC xenograft models, we demonstrated that circRACGAP1 functioned as an endogenous sponge for miR-3657 to inhibit its activity and further upregulate ATG7 expression. Silencing of circRACGAP1 inhibited apatinib-induced autophagy, which was rescued by miR-3657. Moreover, knockdown of circRACGAP1 sensitized GC cells to apatinib via autophagy inhibition in vitro and in vivo. These findings provided the first evidence that the circRACGAP1-miR-3657-ATG7 axis mediates a novel regulatory pathway critical for the regulation of apatinib sensitivity in GC. Thus, specific blockage of circRACGAP1 may be a potential therapeutic strategy to reduce the toxicities of apatinib and enhance its therapeutic effect in human GC.

Indexed as

AutophagyAutophagy-Related Protein 7Cell Line, TumorHumansRNA, CircularSignal TransductionStomachATG7 protein, humanAutophagy-Related Protein 7RNA, Circular

Identifiers

PMID32139670
PMCPMC7058073
OpenAlexW3010206004

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.