Evidence map›Paper›PMID 36056690›Full record

ArticleJournal of cellular and molecular medicine2022

SNORA70E promotes the occurrence and development of ovarian cancer through pseudouridylation modification of RAP1B and alternative splicing of PARPBP.

Shuo Chen, Qian-Hui Li, Xi Chen, Hai-Juan Bao, Wu Wu, Fan Shen, Bing-Feng Lu, Ru-Qi Jiang, Zhi-Hong Zong, Yang Zhao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. 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
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

29 citing papers in PubMed, 39 citations in OpenAlex.

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  16. SnoRNAs: The promising targets for anti-tumor therapy.Journal of pharmaceutical analysis · 2024
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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 1 institution in 1 country.

Shuo ChenDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qian-Hui LiDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xi ChenDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Hai-Juan BaoDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Wu WuDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Fan ShenDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Bing-Feng LuDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Ru-Qi JiangDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Zhi-Hong ZongDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yang ZhaoDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0003-3226-8127
Third Affiliated Hospital of Guangzhou Medical University · CN

Funding

Fundamental Research Project of Guangzhou Municipal School (College) Joint Funding (High-level University) 202201020093Fundamental Research Project of Guangzhou Municipal School (College) Joint Funding (High-level University) 202201020118National Natural Science Foundation of China 81872115National Natural Science Foundation of China 82072854Natural Science Foundation of Guangdong Province 2022A1515012293Project for Key Medicine Discipline Construction of Guangzhou Municipality 2021-2023-17Young S&T Talent Training Program of Guangdong Provincial Association for S&T (GDSTA) KXRC202214
6 · The paper itself

Abstract

The present study demonstrated for the first time that SNORA70E, which belongs to box H/ACA small nucleolar noncoding RNAs (snoRNAs) who could bind and induce pseudouridylation of RNAs, was significantly elevated in ovarian cancer tissues and was an unfavourable prognostic factor of ovarian cancer. The over-expression of SNORA70E showed increased cell proliferation, invasion and migration in vitro and induced tumour growth in vivo. Further research found that SNORA70E regulates RAS-Related Protein 1B (RAP1B) mRNA through pseudouracil modification by combing with the pyrimidine synthase Dyskerin Pseudouridine Synthase 1 (DKC1) and increase RAP1B protein level. What's more, the silencing of DKC1/RAP1B in SNORA70E overexpression cells both inhibited cell proliferation, migration and invasion through reducing β-catenin, PI3K, AKT1, mTOR, and MMP9 protein levels. Besides, RNA-Seq results revealed that SNORA70E regulates the alternative splicing of PARP-1 binding protein (PARPBP), leading to the 4th exon-skipping in PARPBP-88, forming a new transcript PARPBP-15, which promoted cell invasion, migration and proliferation. Finally, ASO-mediated silencing of SNORA70E could inhibit ovarian cancer cell proliferation, invasion, migration ability in vitro and inhibit tumorigenicity in vivo. In conclusion, SNORA70E promotes the occurrence and development of ovarian cancer through pseudouridylation modification of RAP1B and alternative splicing of PARPBP. Our results demonstrated that SNORA70E may be a new diagnostic and therapeutic target for ovarian cancer.

Indexed as

DNA-Binding ProteinsOvarian Neoplasmsrap GTP-Binding ProteinsRNA, Small NucleolarAlternative Splicingbeta CateninCell Cycle ProteinsCell Line, TumorFemaleHumansMatrix Metalloproteinase 9Nuclear ProteinsPhosphatidylinositol 3-KinasesPoly(ADP-ribose) Polymerase InhibitorsRNA, MessengerTOR Serine-Threonine Kinasesbeta CateninCell Cycle ProteinsDKC1 protein, humanDNA-Binding ProteinsMatrix Metalloproteinase 9Nuclear ProteinsPARPBP protein, humanPhosphatidylinositol 3-KinasesPoly(ADP-ribose) Polymerase InhibitorsRAP1B protein, humanrap GTP-Binding ProteinsRNA, MessengerRNA, Small NucleolarTOR Serine-Threonine Kinasesalternative splicingovarian cancerpseudouracil modificationRAP1BSNORA70E

Identifiers

PMID36056690
PMCPMC9575132
OpenAlexW4294379436

What OpenQuestion holds

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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.