Evidence map›Paper›PMID 32052576›Full record

ArticleThe Kaohsiung journal of medical sciences2020

Overexpression of tripartite motif containing 26 inhibits non-small cell lung cancer cell growth by suppressing PI3K/AKT signaling.

Jia-Li Tao, Man Luo, Hong Sun, Hong-Mei Zhao, Qing-Song Sun, Zi-Ming Huang

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Advances of E3 ligases in lung cancer.Biochemistry and biophysics reports · 2024
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. GraphSynergy: a network-inspired deep learning model for anticancer drug combination prediction.Journal of the American Medical Informatics Association : JAMIA · 2021
    Article
  12. Article
  13. The Risks of miRNA Therapeutics: In a Drug Target Perspective.Drug design, development and therapy · 2021
    Review
  14. Article
  15. 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

6 authors at 1 institution in 1 country.

Jia-Li TaoDepartment of Emergency, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.ORCID https://orcid.org/0000-0002-0670-1567
Man LuoDepartment of Emergency, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Hong SunDepartment of Emergency, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Hong-Mei ZhaoDepartment of Emergency, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Qing-Song SunDepartment of Emergency, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Zi-Ming HuangDepartment of Emergency Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, China.ORCID https://orcid.org/0000-0002-7654-1335
Xuzhou Medical College · CN

Funding

The General Project of Science and Technology Development Fund of Nanjing Medical University 2013NJMU225
6 · The paper itself

Abstract

It has been reported that tripartite motif containing 26 (TRIM26) is involved in the tumorigenesis of some cancers, but its function in non-small cell lung cancer (NSCLC) is still unclear. In this study, we found that TRIM26 was markedly down-regulated in both of NSCLC tumor tissues and cell lines. Additionally, high expression of TRIM26 in NSCLC patients predicted a positive index for patients' overall survival. What is more, overexpression of TRIM26 significantly suppressed NSCLC cell growth. Our further studies indicated that overexpression of TRIM26 inhibited the phosphorylation of PI3K p85 and AKT. And overexpressed TRIM26 regulated cell cycle-related genes' expression, including downregulating CDK4, Cyclin A, Cyclin D1, Cyclin D3, and Cyclin E, and upregulating p27 expression. Finally, we found that TRIM26 up-regulated PTEN expression by stabilizing PTEN protein in NSCLC cells. Collectively, our present study indicated that TRIM26 was decreased in NSCLC and overexpression of TRIM26 inhibited NSCLC cell growth by suppressing PI3K/AKT pathway, which suggested that TRIM26 could be as a potential target for the treatment of NSCLC in the future.

Indexed as

A549 CellsCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationClass Ia Phosphatidylinositol 3-KinaseCyclin ACyclin D1Cyclin D3Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin EGene Expression Regulation, NeoplasticHumansLung NeoplasmsCCND1 protein, humanCCND3 protein, humanCDK4 protein, humanClass Ia Phosphatidylinositol 3-KinaseCyclin ACyclin D1Cyclin D3Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin EProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTRIM26 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesAKTcell growthnon-small cell lung cancerPTENTRIM26

Identifiers

PMID32052576
PMCPMC11896303
OpenAlexW3005668498

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.