Evidence map›Paper›PMID 35220277›Full record

ArticleAging2022

Pseudogene AK4P1 promotes pancreatic ductal adenocarcinoma progression through relieving miR-375-mediated YAP1 degradation.

Lang Jia, Yun Zhang, Feng Pu, Chong Yang, Shula Yang, Jinze Yu, Zihan Xu, Hongji Yang, Yu Zhou, Shikai Zhu

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

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. 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 1 institution in 1 country.

Lang JiaOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Yun ZhangOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Feng PuOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Chong YangOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Shula YangOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Jinze YuOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Zihan XuOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Hongji YangOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Yu ZhouHuman Disease Gene Study Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
Shikai ZhuOrgan Transplant Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
University of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogenes have been reported to play oncogenic or tumor-suppressive roles in cancer progression. However, the molecular mechanism of most pseudogenes in pancreatic ductal adenocarcinoma (PDAC) remains unknown. Herein, we characterized a novel pseudogene-miRNA-mRNA network associated with PDAC progression using bioinformatics analysis. After screening by dreamBase and GEPIA, 12 up-regulated and 7 down-regulated differentially expressed pseudogenes (DEPs) were identified. According to survival analysis, only elevated AK4P1 indicated a poor prognosis for PDAC patients. Moreover, we found that AK4 acts as a cognate gene of AK4P1 and also predicts worse survival for PDAC patients. Furthermore, 32 miRNAs were predicted to bind to AK4P1 by starBase, among which miR-375 was identified as the most potential binding miRNA of AK4P1. A total of 477 potential target genes of miR-375 were obtained by miRNet, in which 49 hub genes with node degree ≥ 20 were identified by STRING. Subsequent analysis for hub genes demonstrated that YAP1 may be a functional downstream target of AK4P1. To confirmed the above findings, microarray, and qRT-PCR assay revealed that YAP1 was dramatically upregulated in both PDAC cells and tissues. Functional experiments showed that knockdown of YAP1 significantly suppressed PDAC cells growth, increased apoptosis, and decreased the ability of invasion. In conclusion, amplification of AK4P1 may fuel the onset and development of PDAC by targeting YAP1 through competitively binding to miR-375, and serve as a promising biomarker and therapeutic target for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalMicroRNAsPancreatic NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPrognosisPseudogenesYAP-Signaling ProteinsMicroRNAsMIRN375 microRNA, humanYAP1 protein, humanYAP-Signaling ProteinsAK4P1ceRNAmiR-375pancreatic ductal adenocarcinomapseudogene

Identifiers

PMID35220277
PMCPMC8908928
OpenAlexW4214542344

What Socratic 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 Socratic graph.