Evidence map›Paper›PMID 27129164›Full record

ArticleOncotarget2016

SUMOylation of TBL1 and TBLR1 promotes androgen-independent prostate cancer cell growth.

Soo-Yeon Park, Younghwa Na, Mee-Hee Lee, Jae-Sung Seo, Yoo-Hyun Lee, Kyung-Chul Choi, Hyo-Kyoung Choi, Ho-Geun Yoon

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
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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 5 institutions in 1 country.

Soo-Yeon ParkDepartment of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seodaemun-gu, Seoul, South Korea.
Younghwa NaCollege of Pharmacy, CHA University, Gyeonggi-do, Pocheon, South Korea.
Mee-Hee LeeDepartment of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seodaemun-gu, Seoul, South Korea.
Jae-Sung SeoDepartment of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seodaemun-gu, Seoul, South Korea.
Yoo-Hyun LeeDepartment of Food Science and Nutrition, The University of Suwon, Kyunggi-do, South Korea.
Kyung-Chul ChoiDepartment of Biomedical Sciences, University of Ulsan College of Medicine, Poongnap-dong, Songpa-gu, Seoul, South Korea.
Hyo-Kyoung ChoiDivision of Nutrition and Metabolism Research Group, Korea Food Research Institute, Gyeonggi-do, South Korea.
Ho-Geun YoonDepartment of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seodaemun-gu, Seoul, South Korea.
Yonsei University · KRCHA University · KRKorea Food Research Institute · KRUlsan College · KRUniversity of Suwon · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation is strongly associated with prostate cancer pathogenesis. Transducin β-like protein (TBL1) and Transducin β-like 1X-linked receptor 1 (TBLR1) have been identified recently as a coactivator for NF-κB-mediated transcription; however, the underlying mechanism by which TBL1 and TBLR1 activate NF-κB function during inflammation remains unknown. Here, we demonstrate that cytokine production is significantly elevated in androgen-independent PC-3 prostate cancer cells compared with androgen-dependent LNCaP prostate cancer cells. Elevated cytokine production positively correlates with the TBL1 and TBLR1 SUMOylation level in PC-3 cells. We show that both TBL1 and TBLR1 are SUMOylated in response to TNF-α treatment, and this increases formation of the TBL1-TBLR1-NF-κB complex, which leads to NF-κB-mediated transcriptional activation of cytokine gene expression. Conversely, SENP1-mediated deSUMOylation of TBL1 and TBLR1 inhibits NF-κB-target gene expression by dissociating TBL1 and TBLR1 from the nuclear hormone receptor corepressor (NCoR) complex. TBL1 knockdown substantially suppresses inflammatory signaling and PC-3 cell proliferation. Collectively, these results suggest that targeted SUMOylation of TBL1 and TBLR1 may be a useful strategy for therapeutic treatment of androgen-independent prostate cancer.

Indexed as

Cell ProliferationSumoylationAndrogensCell Line, TumorCytokinesHumansInflammation MediatorsMaleNuclear ProteinsProstatic NeoplasmsReceptors, Cytoplasmic and NuclearRepressor ProteinsTransducinAndrogensCytokinesInflammation MediatorsNuclear ProteinsReceptors, Cytoplasmic and NuclearRepressor ProteinsTBL1X protein, humanTBL1XR1 protein, humanTransducininflammationNF-κBSUMOylationTBL1TBLR1

Identifiers

PMID27129164
PMCPMC5173046
OpenAlexW2344018144

What OpenQuestion 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 OpenQuestion graph.