Evidence map›Paper›PMID 32810693›Full record

ArticleMolecular therapy. Nucleic acids2020

RP11-480I12.5-004 Promotes Growth and Tumorigenesis of Breast Cancer by Relieving miR-29c-3p-Mediated AKT3 and CDK6 Degradation.

Weiyang Lou, Bisha Ding, Guansheng Zhong, Jia Yao, Weimin Fan, Peifen Fu

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  13. Veterinary sciences · 2022
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  15. Review
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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

6 authors at 1 institution in 1 country.

Weiyang LouDepartment of Breast Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, Zhejiang 310003, China; Program of Innovative Cancer Therapeutics, Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, College of Medicine, Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Key Laboratory of Organ Transplantation, Zhejiang University, Hangzhou 310003, Zhejiang, Province, China. Electronic address: 11718264@zju.edu.cn.
Bisha DingProgram of Innovative Cancer Therapeutics, Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, College of Medicine, Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Key Laboratory of Organ Transplantation, Zhejiang University, Hangzhou 310003, Zhejiang, Province, China.
Guansheng ZhongDepartment of Breast Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, Zhejiang 310003, China.
Jia YaoDepartment of Breast Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, Zhejiang 310003, China.
Weimin FanProgram of Innovative Cancer Therapeutics, Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, College of Medicine, Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Key Laboratory of Organ Transplantation, Zhejiang University, Hangzhou 310003, Zhejiang, Province, China.
Peifen FuDepartment of Breast Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, Zhejiang 310003, China. Electronic address: Peifen_Fu@163.com.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogenes have been reported to exert oncogenic or tumor-suppressive functions in cancer. However, the expression, role, and mechanism of pseudogene-derived RNAs in breast cancer remain unclear. The RNA levels and prognostic values of pseudogenes in breast cancer were determined. The levels of RP11-480I12.5 in cell lines and clinical samples were validated by quantitative real-time PCR. In vitro effects of RP11-480I12.5 on cell growth were measured by cell counting kit-8 (CCK-8) assay, colony formation assay, cell counting assay, and flow cytometry analysis. Xenograft model was established to detect its in vivo effect. The potential mechanism of RP11-480I12.5 was also studied by a combination of bioinformatic analysis and experimental confirmation. Finally, the possible functional parental genes of RP11-480I12.5 in breast cancer were explored. After a series of bioinformatic analyses, RP11-480I12.5 was selected as the most potential pseudogene in breast cancer. RP11-480I12.5 expression was significantly upregulated in breast cancer cell lines and clinical breast cancer tissues. Knockdown of RP11-480I12.5 markedly suppressed cell proliferation and colony formation, induced cell apoptosis of breast cancer in vitro, and inhibited tumor growth in vivo. Four transcripts of RP11-480I12.5 (001/002/003/004) were identified. Only overexpression of RP11-480I12.5-004 significantly enhanced cell growth of breast cancer both in vitro and in vivo. RP11-480I12.5-004 mainly located in cytoplasm and increased AKT3 and CDK6 mRNA expression, at least in part, by competitively binding to miR-29c-3p. Six parental genes of RP11-480I12.5 were found, among which TUBA1B and TUBA1C were statistically linked to RP11-480I12.5 expression, possessed prognostic values, and were upregulated in breast cancer. Our findings suggested that pseudogene-derived long non-coding RNA (lncRNA) RP11-480I12.5-004 promoted growth and tumorigenesis of breast cancer via increasing AKT3 and CDK6 expression by competitively binding to miR-29c-3p.

Indexed as

AKT3breast cancerCDK6lncRNAlong non-coding RNAmicroRNAmiR-29c-3pmiRNApseudogeneRP11-480I12.5-004

Identifiers

PMID32810693
PMCPMC7452110
OpenAlexW3045323304

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.