Evidence map›Paper›PMID 35768649›Full record

ArticleHuman cell2022

TRIM36 suppresses cell growth and promotes apoptosis in human esophageal squamous cell carcinoma cells by inhibiting Wnt/β-catenin signaling pathway.

Bin Zhao, Gaofeng Qiao, Jianhua Li, Yukun Wang, XiaoDong Li, Hua Zhang, Lu Zhang

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. iScience · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Multifaceted role ofMedComm · 2024
    Review
  8. Review
  9. Advances in the antitumor mechanisms of tripartite motif-containing protein 3.Journal of cancer research and clinical oncology · 2024
    Review
  10. Article
  11. Article
  12. 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 3 institutions in 1 country.

Bin Zhao *Department of Thoracic Surgery, Shandong Provincial Public Health Clinical Center, Jinan, China.
Gaofeng Qiao *Department of Thoracic Surgery, Shandong Provincial Public Health Clinical Center, Jinan, China.
Jianhua LiDepartment of Thoracic Surgery, Qingdao ChengYang People's Hospital, Qingdao, China.
Yukun WangDepartment of Internal Medicine, The Third Affiliated Hospital of Shandong First Medical University (Affiliated Hospital of Shandong Academy of Medical Sciences), Taian, China.
XiaoDong LiDepartment of Thoracic Surgery, Shandong Provincial Public Health Clinical Center, Jinan, China.
Hua ZhangDepartment of Thoracic Surgery, Shandong Provincial Public Health Clinical Center, Jinan, China. 95192789@qq.com.
Lu ZhangDepartment of Cardiothoracic Surgery, Affiliated Kunshan Hospital of Jiangsu University, Zhenjiang, China. zhangl_u868@163.com.
Shanghai Public Health Clinical Center · CNJiangsu University · CNShandong First Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our recent study has shown that TRIM36, a member of tripartite motif-containing (TRIM) family proteins and tumor suppressor and β-catenin may serve as a prognostic biomarker for esophageal squamous cell carcinoma (ESCC). Here, we sought to examine functional roles of TRIM36 and β-catenin in ESCC cells. TRIM36 was overexpressed or silenced by lentivirus transduction. Cell proliferation was examined by Cell Counting Kit (CCK)-8 assay, while cell cycle distribution and cell apoptosis was assessed via flow cytometry analysis. Xenograft mouse model was applied for in vivo analysis. Overexpression of TRIM36 inhibited cell proliferation in human ESCC cells, and silencing of TRIM36 led to opposite effects. We also found that ectopic expression of TRIM36 enhanced the ratio of G0/G1 phase cells and induced apoptosis in ESCC cells. Our data further revealed that TRIM36 stimulated the ubiquitination of β-catenin, and in turn, its inactivation. Finally, we confirmed these in vitro results in a xenograft mouse model and clinical specimens post-operatively obtained from patients of ESCC. In summary, these data support that TRIM36 can effectively inhibit tumorigenesis of ESCC by repressing Wnt/β-catenin signaling pathway, which suggest that selectively repressing this signaling pathway in ESCC may lead to development of a novel therapeutic approach for controlling this disease.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsApoptosisbeta CateninCarrier ProteinsCell CycleCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHeterograftsHumansMiceTripartite Motif ProteinsUbiquitin-Protein Ligasesbeta CateninCarrier ProteinsTRIM36 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesApoptosisEsophageal cancerTRIM36Ubiquitinationβ-Catenin

Identifiers

PMID35768649
OpenAlexW4283707076

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.