Evidence map›Paper›PMID 32439863›Full record

ArticleOncogene2020

PPARδ is a regulator of autophagy by its phosphorylation.

Qian Gou, Yidan Jiang, Runyun Zhang, Ying Xu, Huihui Xu, Wenbo Zhang, Juanjuan Shi, Yongzhong Hou

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Ubiquitination of CD47 Regulates Innate Anti-Tumor Immune Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Inhibition of CK2/ING4 Pathway Facilitates Non-Small Cell Lung Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Role of autophagy on cancer immune escape.Cell communication and signaling : CCS · 2021
    Review
  12. Review
  13. Review
  14. Review
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

8 authors at 1 institution in 1 country.

Qian Gou *Institute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Yidan Jiang *Institute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Runyun Zhang *Institute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Ying XuInstitute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Huihui XuInstitute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Wenbo ZhangInstitute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Juanjuan ShiInstitute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.
Yongzhong HouInstitute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China. houyz@ujs.edu.cn.ORCID http://orcid.org/0000-0003-2019-8686
Jiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to nutrient deficiency, autophagy degrades cytoplasmic materials and organelles in lysosomes, which is nutrient recycling, whereas activation of EGFR mediates autophagy suppression in response to growth factors. It is unclear whether PPARδ could be the regulator of autophagy in response to active EGFR. Here we found that EGFR induced PPARδ phosphorylation at tyrosine-108 leading to increased binding of LC3 to PPARδ by its LIR (LC3 interacting region) motif, consequently, inhibited autophagic flux. Conversely, EGFR inhibitor treatment reversed this event. Furthermore, EGFR-mediated PPARδ phosphorylation at tyrosine-108 led to autophagy inhibition and tumor growth. These findings suggest that PPARδ serves as a regulator of autophagy by its phosphorylation.

Indexed as

AutophagyCell Line, TumorEpidermal Growth FactorErbB ReceptorsGefitinibHCT116 CellsHumansMicrotubule-Associated ProteinsMutationPhosphorylationPPAR deltaProtein BindingProtein Kinase InhibitorsTyrosineEGFR protein, humanEpidermal Growth FactorErbB ReceptorsGefitinibMAP1LC3A protein, humanMicrotubule-Associated ProteinsPPAR deltaProtein Kinase InhibitorsTyrosine

Identifiers

PMID32439863
OpenAlexW3026367747

What OpenQuestion holds

Textmetadata
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.