Evidence map›Paper›PMID 34353336›Full record

ArticleJournal of translational medicine2021

MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54.

Bolong Liu, Pingbo Yao, Feng Xiao, Jianjin Guo, Lianghui Wu, Yong Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023
    Review
  8. Review
  9. [High expression of MYBL2 promotes progression and predicts a poor survival outcome of prostate cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  10. Article
  11. Article
  12. Article
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 4 institutions in 1 country.

Bolong LiuDepartment of Andrology, The First Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, China.
Pingbo YaoChangsha Social Work College, Changsha, 421004, Hunan, China.
Feng XiaoDepartment of Oncology, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Jianjin GuoDepartment of Endocrinology and Metabolism, The Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Lianghui WuDepartment of Intensive Care Unit, Affiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road, Zhuhui District, Hengyang, 421001, Hunan, China. wulianghui20051217@163.com.
Yong YangDepartment of General Surgery, The Second Hospital, University of South China, 30 Jiefang Road, Shigu District, Hengyang, 421001, Hunan, China. maji1177@sina.com.
University of South China · CNChangsha University · CNSecond Hospital of Shanxi Medical University · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn recent years, long non-coding RNAs (lncRNAs) have attracted much attention because of its regulatory role in occurrence and progression of tumors, including triple-negative breast cancer (TNBC). LncRNA PITPNA antisense RNA 1 (PITPNA-AS1) has been explored in some cancers, whereas its function and molecular mechanism in TNBC remain unclear.

methodsPITPNA-AS1 expression in TNBC tissues and cells was determined by RT-qPCR. TNBC cell viability, proliferation, migration, invasion were assessed with CCK-8, colony formation, wound healing, transwell assays. Cell apoptosis was evaluated by flow cytometry. Expression of EMT-related markers was detected by western blot analyses. The molecular mechanism of PITPNA-AS1 was explored by RNA pull down, luciferase reporter, RIP and ChIP assays.

resultsPITPNA-AS1 showed high expression levels in TNBC tissues and cells. PITPNA-AS1 knockdown suppressed TNBC cell viability, proliferation, migration, invasion in vitro and inhibited xenograft tumor growth in mice. Mechanistically, PITPNA-AS1 upregulated SIK2 expression by sponging miR-520d-5p and recruiting DDX54 protein. Results of rescue assays suggested that the inhibitive effects of silenced PITPNA-AS1 on TNBC cellular processes were partially rescued by overexpressing SIK2 or combination of miR-520d-5p inhibition and DDX54 overexpression. More importantly, we found that the upregulation of PITPNA-AS1 in TNBC cells was attributed to transcription factor MYBL2.

conclusionPITPNA-AS1 activated by MYBL2 plays an oncogenic role in TNBC through upregulating SIK2.

Indexed as

MicroRNAsRNA, Long NoncodingTriple Negative Breast NeoplasmsAnimalsCell Cycle ProteinsCell ProliferationDEAD-box RNA HelicasesDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceNeoplasm ProteinsTrans-ActivatorsCell Cycle ProteinsDDX54 protein, humanDEAD-box RNA HelicasesMicroRNAsMYBL2 protein, humanNeoplasm ProteinsRNA, Long NoncodingTrans-ActivatorsDDX54miR-520d-5pPITPNA-AS1SIK2TNBC

Identifiers

PMID34353336
PMCPMC8340450
OpenAlexW3192389726

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.