Evidence map›Paper›PMID 36266728›Full record

ArticleClinical epigenetics2022

PDCD5 inhibits progression of renal cell carcinoma by promoting T cell immunity: with the involvement of the HDAC3/microRNA-195-5p/SGK1.

Shu-Cheng Liu, Li-Bo Chen, Ping-Feng Chen, Meng-Long Huang, Tian-Pei Liu, Jun Peng, Xin-Sheng Lu

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

Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  5. Review
  6. 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

7 authors at 1 institution in 1 country.

Shu-Cheng LiuThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Li-Bo ChenThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Ping-Feng ChenThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Meng-Long HuangThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Tian-Pei LiuThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.
Jun PengThe First Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. 409195150@qq.com.
Xin-Sheng LuThe First Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China. 4755397@qq.com.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpigenetics exerts a vital role in the onset and development of renal cell carcinoma (RCC). Mounting evidence has shed light on the significance of human immune system in response to tumor infiltrating T cells. Hereby, we sought to unmask the immunomodulatory role of histone deacetylase 3 (HDAC3) and its potential upstream molecule, programmed cell death 5 (PDCD5) in RCC.

methodsRCC and adjacent non-cancerous tissues were clinically resected from 58 patients, in which the expression profile of microRNA-195-5p (miR-195-5p), PDCD5, HDAC3, and serum glucocorticoid-inducible kinase 1 (SGK1) was determined by RT-qPCR and Western blot analysis. Their relations were investigated by a series of luciferase assays in combination with ChIP and co-IP. RCC cells (A498) were intervened using gain- and loss-of-function approaches, followed by cell proliferation evaluation. After co-culture with CD3

resultsPDCD5 was downregulated in RCC tissues and A498 cells. Upregulation of HDAC3, as well as of SGK1, resulted in suppression of A498 cell proliferation and promotion of T cell activation as evidenced by higher IFN-γ expression. Re-expression of PDCD5 downregulated HDAC3, causing a subsequent upregulation of miR-195-5p, while miR-195-5p could inversely modulate its target gene, SGK1. The regulatory mechanism appeared to be functional in vivo.

conclusionOur results highlight the possible manipulation by PDCD5 on RCC cell proliferation and T cell activation, which provides new clues to better understand the immune balance in RCC progression.

Indexed as

Apoptosis Regulatory ProteinsCarcinoma, Renal CellKidney NeoplasmsMicroRNAsNeoplasm ProteinsAnimalsCell Line, TumorDNA MethylationHistone Deacetylase 3HumansInterferon-gammaMiceSerum-Glucocorticoid Regulated KinasesT-LymphocytesApoptosis Regulatory ProteinsHistone Deacetylase 3Interferon-gammaMicroRNAsMIRN195 microRNA, humanNeoplasm ProteinsPDCD5 protein, humanSerum-Glucocorticoid Regulated KinasesHistone deacetylase 3microRNA-195-5pProgrammed cell death 5Renal cell carcinomaSerum glucocorticoid-inducible kinase 1

Identifiers

PMID36266728
PMCPMC9583501
OpenAlexW4306874545

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.