Evidence map›Paper›PMID 31581131›Full record

ArticleAging2019

SNHG22 overexpression indicates poor prognosis and induces chemotherapy resistance via the miR-2467/Gal-1 signaling pathway in epithelial ovarian carcinoma.

Peng-Fei Zhang, Jing Wu, Jin-Hong Luo, Ke-Sang Li, Fei Wang, Wei Huang, Yin Wu, Shui-Ping Gao, Xue-Mei Zhang, Peng-Nan Zhang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 52 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

10 authors at 3 institutions in 1 country.

Peng-Fei ZhangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jing WuDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jin-Hong LuoDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Ke-Sang LiDepartment of Hematology and Oncology, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, China.
Fei WangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Wei HuangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yin WuDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shui-Ping GaoDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xue-Mei ZhangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Peng-Nan ZhangDepartment of Gynecology, Obstetrics and Gynecology Hospital of Fudan University, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Shanghai, China.
Shanghai East Hospital · CNObstetrics and Gynecology Hospital of Fudan University · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, an increasing number of studies have reported that dysregulation of long noncoding RNAs (lncRNAs) plays an important role in cancer initiation and progression, including in epithelial ovarian carcinoma (EOC). However, little is known about the detailed biological functions of the lncRNA small nucleolar RNA host gene 22 (SNHG22) during the progression of EOC. Here, we found that SNHG22 was significantly increased in EOC tissues and was significantly associated with a low level of differentiation. Forced SNHG22 expression promoted chemotherapy resistance in EOC cells. Knockdown of SNHG22 expression increased the sensitivity of EOC cells to cisplatin and paclitaxel. Importantly, we found that SNHG22 could directly interact with miR-2467 and lead to the release of miR-2467-targeted Gal-1 mRNA. Moreover, SNHG22 overexpression induced EOC cell resistance to chemotherapy agents via PI3K/AKT and ERK cascade activation. In summary, our findings demonstrate that SNHG22 plays a critical role in the chemotherapy resistance of EOC by mediating the miR-2467/Gal-1 regulatory axis.

Indexed as

Antineoplastic AgentsBiomarkers, TumorCarcinoma, Ovarian EpithelialCisplatinDisease ProgressionDrug Resistance, NeoplasmFemaleGalectin 1Gene Expression Regulation, NeoplasticHumansMicroRNAsMiddle AgedOvarian NeoplasmsPaclitaxelPrognosisRNA, Long NoncodingAntineoplastic AgentsBiomarkers, TumorCisplatinGalectin 1LGALS1 protein, humanMicroRNAsMIRN2467 microRNA, humanPaclitaxelRNA, Long Noncodingchemoresistanceepithelial ovarian carcinomagalectin-1long-noncoding RNA

Identifiers

PMID31581131
PMCPMC6814594
OpenAlexW2977474566

What OpenQuestion holds

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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.