Evidence map›Paper›PMID 35478990›Full record

ArticleDisease markers2022

Long Noncoding RNA TFAP2A-AS1 Suppressed Hepatitis B Virus Replication by Modulating miR-933/HDAC11.

Yu Cheng, Weiwu Shi, Xudong Cui, Lei Sun, Yi Nan, Hong Yao, Jian Fan, LiYing Zhu, Lei Yu

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 40% 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, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Translational cancer research · 2023
    Article
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Yu ChengDepartment of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.
Weiwu ShiDepartment of integrated internal medicine, Shanghai Donghai Senior Nursing Hospital, Shanghai, China.
Xudong CuiDepartment of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.
Lei SunDepartment of Ophthalmology, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.
Yi NanTraditional Chinese Medicine College of Ningxia Medical University, Yinchuan 750004, China.
Hong YaoDepartment of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.
Jian FanDepartment of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.
LiYing ZhuDepartment of Infectious Disease, The Second Hospital of Harbin Medical University, Harbin, 150000 Heilongjiang, China.ORCID https://orcid.org/0000-0002-5948-0227
Lei YuDepartment of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin, 150001 Heilongjiang, China.ORCID https://orcid.org/0000-0002-8606-3373
Harbin Medical University · CNNingxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Studies have shown that long noncoding RNAs (lncRNAs) play crucial roles in multiple tumor types and regulate various biological processes. The present study tried to study lncRNA TFAP2A-AS1 in HBV infection hepatocellular carcinoma. Methods: The level of TFAP2A-AS1 and miR-933 in HCC cell and samples were detected by qRT-PCR assay. Luciferase reporter gene assay was carried out to study the mechanism of TFAP2A-AS1 and miR-933. Cell proliferation was measured by CCK-8 assay. HBV DNA replication was detected by RT-qPCR. Results: We firstly demonstrated that TFAP2A-AS1 was downregulated in HCC cell lines and HBV-infected HCC samples compared with nontumor tissues. However, miR-933 was upregulated in HCC cell lines and HBV-infected HCC samples compared with nontumor tissues, and miR-933 was negatively associated with the expression of TFAP2A-AS1 in HBV-correlated HCC samples. TFAP2A-AS1 and HDAC11 expression was decreased and miR-933 was upregulated in the HBV-infected cell HepG2.2.15. TFAP2A-AS1 acted as a sponge for miR-933 and HDAC11 was one direct target gene for miR-933. Overexpression of TFAP2A-AS1 suppressed cell growth, HBV DNA replication, HbeAg, and HbsAg expression, while knockdown of TFAP2A-AS1 enhanced cell proliferation, HBV DNA replication, HbeAg, and HbsAg expression in HepG2.2.15 cell. In addition, ectopic expression of miR-933 promoted cell growth, HBV DNA replication, HbeAg, and HbsAg expression in HepG2.2.15 cell. TFAP2A-AS1 suppressed HBV replication and infection through regulating HDAC11. Conclusion: These data demonstrated that TFAP2A-AS1 acted crucial roles in the modulation of HbeAg and HbsAg expression and HBV replication and may be one potential target for HBV infection treatment.

Indexed as

Carcinoma, HepatocellularHepatitis BLiver NeoplasmsMicroRNAsRNA, Long NoncodingGene Expression Regulation, NeoplasticHepatitis B e AntigensHepatitis B Surface AntigensHepatitis B virusHistone DeacetylasesHumansTranscription Factor AP-2Virus ReplicationHDAC11 protein, humanHepatitis B e AntigensHepatitis B Surface AntigensHistone DeacetylasesMicroRNAsRNA, Long NoncodingTFAP2A protein, humanTranscription Factor AP-2

Identifiers

PMID35478990
PMCPMC9038435
OpenAlexW4224287933

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.