Evidence map›Paper›PMID 33522895›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

SP1 induced long non-coding RNA AGAP2-AS1 promotes cholangiocarcinoma proliferation via silencing of CDKN1A.

Hao Ji, Juan Wang, Binbin Lu, Juan Li, Jing Zhou, Li Wang, Shufen Xu, Peng Peng, Xuezhen Hu, Keming Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024
    Review
  5. Article
  6. Article
  7. 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

10 authors at 2 institutions in 1 country.

Hao Ji *Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Juan Wang *Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Binbin Lu *Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Juan LiDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Jing ZhouDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Li WangDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Shufen XuDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Peng PengDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China.
Xuezhen HuJiangsu Provincial Hospital of Traditional Chinese Medicine, Nanjing, China. Njhxzh@126.com.
Keming WangDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China. kemingwang@njmu.edu.cn.ORCID 0000-0003-1513-9884
Second Affiliated Hospital of Nanjing Medical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration.

methodsWe investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1.

resultsAGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA.

conclusionsWe conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.

Indexed as

Up-RegulationAnimalsBile Duct NeoplasmsCell Line, TumorCell ProliferationCholangiocarcinomaFemaleGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm TransplantationRNA, Long NoncodingSp1 Transcription Factorlong non-coding RNA AGAP2-AS1, humanRNA, Long NoncodingSP1 protein, humanSp1 Transcription FactorAGAP2-AS1Biomarker apoptosisCCAEZH2LncRNA

Identifiers

PMID33522895
PMCPMC7852216
OpenAlexW3126803394

What OpenQuestion holds

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LicenceCC BY
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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.