Evidence map›Paper›PMID 26676636›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Upregulated SMYD3 promotes bladder cancer progression by targeting BCLAF1 and activating autophagy.

Bing Shen, Mingyue Tan, Xinyu Mu, Yan Qin, Fang Zhang, Yong Liu, Yu Fan

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  9. Frontiers in pharmacology · 2024
    Article
  10. Function of BCLAF1 in human disease.Oncology letters · 2022
    Review
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  12. 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

7 authors at 1 institution in 1 country.

Bing ShenDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Mingyue TanDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Xinyu MuDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Yan QinDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Fang ZhangDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Yong LiuDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China.
Yu FanDepartment of Renal Transplantation and Urology, Shanghai First People's Hospital, Shanghai Jiaotong University, 100 Haining Road, Shanghai, 200080, China. fanyu1965@163.com.
Shanghai First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent discovery of a large number of histone methyltransferases reveals important roles of these enzymes in regulating tumor development and progression. SMYD3, a histone methyltransferase, is associated with poor prognosis of patients with prostate and gastric cancer. In the study, we attempted to investigate its putative oncogenic role on bladder cancer. Here, we report that SMYD3 frequently amplified in bladder cancer is correlated with bladder cancer progression and poor prognosis. Overexpression of SMYD3 promotes bladder cancer cell proliferation and invasion, whereas SMYD3 knockdown inhibits cancer cell growth and invasion. Mechanically, SMYD3 positively regulates the expression of BCL2-associated transcription factor 1 (BCLAF1). SMYD3 physically interacts with the promoter of BCLAF1 and upregulates its expression by accumulating di- and trimethylation of H3K4 at the BCLAF1 locus. We further show that SMYD3 overexpression in bladder cancer cells promotes autophagy activation, whereas BCLAF1 depletion inhibits SMYD3-induced autophagy. Finally, we demonstrate that SMYD3 promotes bladder cancer progression, at least in part by increasing BCLAF1 expression and activating autophagy. Our results establish a function for SMYD3 in autophagy activation and bladder cancer progression and suggest its candidacy as a new prognostic biomarker and target for clinical management of bladder cancer.

Indexed as

AgedAutophagyCarcinoma, Transitional CellCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHistone CodeHistone-Lysine N-MethyltransferaseHistonesHumansMaleMethylationMiddle AgedNeoplasm InvasivenessNeoplasm ProteinsBCLAF1 protein, humanHistone-Lysine N-MethyltransferaseHistonesNeoplasm ProteinsRecombinant Fusion ProteinsRepressor ProteinsSMYD3 protein, humanTumor Suppressor ProteinsAutophagyBCLAF1Bladder cancerHistone methyltransferasesSMYD3

Identifiers

PMID26676636
OpenAlexW2200004434

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.