Evidence map›Paper›PMID 29196913›Full record

ArticleBreast cancer (Tokyo, Japan)2018

UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer.

Jing He, Yuanping Chen, Lu Cai, Zelei Li, Xiaoqing Guo

Open access · hybridAbstract read
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  9. OGT controls mammalian cell viability by regulating the proteasome/mTOR/ mitochondrial axis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  10. Review
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  15. Ubiquitin Binding Protein 2-Like (UBAP2L): is it so NICE After All?Frontiers in cell and developmental biology · 2022
    Review
  16. Article
  17. Article
  18. The Emerging Role of Stress Granules in Hepatocellular Carcinoma.International journal of molecular sciences · 2021
    Review
  19. 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

5 authors at 2 institutions in 1 country.

Jing HeDepartment of Oncology, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Ganzhou, 341000, Jiangxi, China.
Yuanping ChenDepartment of Oncology, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Ganzhou, 341000, Jiangxi, China.
Lu CaiDepartment of Oncology, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Ganzhou, 341000, Jiangxi, China.
Zelei LiDepartment of Oncology, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Ganzhou, 341000, Jiangxi, China.
Xiaoqing GuoDepartment of Oncology, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Ganzhou, 341000, Jiangxi, China. guoxiaoQ_0102@126.com.
Nanchang University · CNGanzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUbiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer. Thus, this study was designed to evaluate whether UBAP2L can serve as a potential molecular target for breast cancer therapy.

methodsThe expression of UBAP2L was determined in breast cancer tissues and cell lines by Western blotting and Oncomine database mining. Then the expression of UBAP2L was silenced using RNA interference and the effects of UBAP2L knockdown on breast cancer cell proliferation and cell cycle progression by MTT and colony formation assay, and Flow cytometry, respectively.

resultsWe found the expression of UBAP2L was significantly up-regulated in breast cancer tissues and cell lines. Knockdown of UBAP2L suppressed cell proliferation, impaired colony formation ability and induced cell cycle arrest at G2/M phase. At molecular levels, knockdown of UBAP2L increased p21 expression, but decreased the expression of CDK1 and Cyclin B1 in breast cancer cells.

conclusionOur findings suggest that UBAP2L plays an important role in breast cancer cell proliferation and might serve as a potential target for breast cancer treatment.

Indexed as

Cell Cycle CheckpointsCell DivisionCell ProliferationG2 PhaseBiomarkers, TumorBreast NeoplasmsCarrier ProteinsCase-Control StudiesFemaleHumansPrognosisRNA, Small InterferingBiomarkers, TumorCarrier ProteinsRNA, Small InterferingUbap2L protein, humanBreast cancerCDK1Cell proliferationCyclin B1G2/M phaseUBAP2L

Identifiers

PMID29196913
PMCPMC5818569
OpenAlexW2773821608

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.