Evidence map›Paper›PMID 26164001›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

SUMO-specific protease 6 promotes gastric cancer cell growth via deSUMOylation of FoxM1.

Jiu-Gang Song, Hua-Hong Xie, Nan Li, Kai Wu, Ji-Gang Qiu, Da-Ming Shen, Chun-Jin Huang

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. SUMO and the robustness of cancer.Nature reviews. Cancer · 2017
    Review
  6. Article
  7. Trichostatin A potentiates TRAIL-induced antitumor effects via inhibition of ERK/FOXM1 pathway in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Jiu-Gang SongDepartment of Gastroenterology, The 309th Hospital of Chinese People's Liberation Army, Beijing, People's Republic of China.
Hua-Hong XieState Key Laboratory of Cancer Biology, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, People's Republic of China.
Nan LiDepartment of Gastroenterology, The 309th Hospital of Chinese People's Liberation Army, Beijing, People's Republic of China.
Kai WuDepartment of Gastroenterology, The 309th Hospital of Chinese People's Liberation Army, Beijing, People's Republic of China.
Ji-Gang QiuDepartment of General Surgery, Huadong Hospital, Fudan University, Shanghai, People's Republic of China. jigangqiu@126.com.
Da-Ming ShenDepartment of General Surgery, Huadong Hospital, Fudan University, Shanghai, People's Republic of China.
Chun-Jin HuangDepartment of General Surgery, Huadong Hospital, Fudan University, Shanghai, People's Republic of China.
Fudan University · CNThe 309th Hospital of Chinese People's Liberation Army · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SUMOylation is a post-translational modification exerted various effects on the target proteins. SUMOylation is a highly dynamic and reversible process, which has been shown to play an important role in tumorigenesis. However, the roles of sentrin/SUMO-specific proteases (SENPs), which mediate the reverse process of SUMOylation, in tumorigenesis remains largely unexplored. Here, we uncover a critical role of SENP6 in promoting gastric cancer cells growth via regulating the deSUMOylation of a transcription factor forkhead box protein M1 (FoxM1). We demonstrated that the mRNA and protein levels were elevated in gastric cancer tissues. Overexpression of SENP6 promoted, while RNA interference depletion of endogenous SENP6 inhibited gastric cancer cells growth and the ability of colony formation. By using biochemical assays, we identified FoxM1 as a novel substrate of SENP6 in gastric cancer cells. Thus, our data suggest that SENP6, which is highly expressed in gastric cancer cells, regulates the transcriptional activity and stability of FoxM1 through deSUMOylation.

Indexed as

CarcinogenesisCell Line, TumorCell ProliferationCysteine EndopeptidasesForkhead Box Protein M1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansProtein Processing, Post-TranslationalRNA, MessengerStomach NeoplasmsSumoylationCysteine EndopeptidasesForkhead Box Protein M1Forkhead Transcription FactorsFOXM1 protein, humanRNA, MessengerSENP6 protein, humanCell growthFoxM1Gastric cancerSENP6SUMOylation

Identifiers

PMID26164001
OpenAlexW948677531

What OpenQuestion holds

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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.