Evidence map›Paper›PMID 35924439›Full record

ArticleCancer science2022

JNK pathway plays a critical role for expansion of human colorectal cancer in the context of BRG1 suppression.

Takaaki Yoshikawa, Akihisa Fukuda, Mayuki Omatsu, Mio Namikawa, Makoto Sono, Yuichi Fukunaga, Tomonori Masuda, Osamu Araki, Munemasa Nagao, Satoshi Ogawa and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 33% 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, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. 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

20 authors at 1 institution in 1 country.

Takaaki YoshikawaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID https://orcid.org/0000-0002-3173-4360
Akihisa FukudaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Mayuki OmatsuDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Mio NamikawaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Makoto SonoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuichi FukunagaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tomonori MasudaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Osamu ArakiDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Munemasa NagaoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Satoshi OgawaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenji MasuoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Norihiro GotoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yukiko HiramatsuDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yu MutaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Motoyuki TsudaDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID https://orcid.org/0000-0003-2873-1449
Takahisa MarunoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuki NakanishiDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kenji KawadaDepartment of Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shigeo TakaishiLaboratory for Malignancy Control Research (DSK Project), Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiroshi SenoDepartment of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JP

Funding

AMED-PRIME 20gm6010022h0003Grants-in-Aid KAKENHI JP19H03639Grants-in-Aid KAKENHI JP21H02902Japan Agency for Medical Research and Development, the Project for Cancer Research and Therapeutic Evolution 19cm0106142h0002Japan Agency for Medical Research and Development, the Project for Cancer Research and Therapeutic Evolution 20cm0106177h0001Japan Agency for Medical Research and Development, the Project for Cancer Research and Therapeutic Evolution 21cm0106283h0001Mitsubishi Foundation 201910037Mitsubishi Foundation 281119Mochida Foundation 2017bvAgNaito Foundation 32924-1Princess Takamatsu Cancer Research Fund 13-24514Princess Takamatsu Cancer Research Fund 17-24924Princess Takamatsu Cancer Research Fund 21-25332Sumitomo Dainippon PharmaTakeda Foundation 201749741Uehara Foundation 201720143
6 · The paper itself

Abstract

Tumor stem cells (TSCs), capable of self-renewal and continuous production of progeny cells, could be potential therapeutic targets. We have recently reported that chromatin remodeling regulator Brg1 is required for maintenance of murine intestinal TSCs and stemness feature of human colorectal cancer (CRC) cells by inhibiting apoptosis. However, it is still unclear how BRG1 suppression changes the underlying intracellular mechanisms of human CRC cells. We found that Brg1 suppression resulted in upregulation of the JNK signaling pathway in human CRC cells and murine intestinal TSCs. Simultaneous suppression of BRG1 and the JNK pathway, either by pharmacological inhibition or silencing of c-JUN, resulted in even stronger inhibition of the expansion of human CRC cells compared to Brg1 suppression alone. Consistently, high c-JUN expression correlated with worse prognosis for survival in human CRC patients with low BRG1 expression. Therefore, the JNK pathway plays a critical role for expansion and stemness of human CRC cells in the context of BRG1 suppression, and thus a combined blockade of BRG1 and the JNK pathway could be a novel therapeutic approach against human CRC.

Indexed as

Colorectal NeoplasmsMAP Kinase Signaling SystemAnimalsApoptosisCell Line, TumorChromatinDNA HelicasesGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesMiceNeoplastic Stem CellsNuclear ProteinsTranscription FactorsChromatinDNA HelicasesJNK Mitogen-Activated Protein KinasesNuclear ProteinsSMARCA4 protein, humanSmarca4 protein, mouseTranscription Factorsapoptosiscolorectal cancerepigeneticsprognosistumor stem cell

Identifiers

PMID35924439
PMCPMC9530857
OpenAlexW4289841019

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.