Evidence map›Paper›PMID 34075691›Full record

ArticleJournal of cellular and molecular medicine2021

The stabilization of yes-associated protein by TGFβ-activated kinase 1 regulates the self-renewal and oncogenesis of gastric cancer stem cells.

Gang Wang, Qikai Sun, Hai Zhu, Yihui Bi, Haixing Zhu, Aman Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022
    Review
  3. Review
  4. Review
  5. Article
  6. 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

6 authors at 2 institutions in 1 country.

Gang WangDepartment of General Surgery, The Fourth Affiliated Hospital of Anhui Medical University, Hefei, China.
Qikai SunDepartment of Hepatobiliary Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Hai ZhuDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Yihui BiSchool of Pharmacy, Anhui Institute of Innovative Drugs, Anhui Medical University, Hefei, China.
Haixing ZhuDepartment of Gastrointestinal Surgery, Anhui Provincial Cancer Hospital, Hefei, China.
Aman XuDepartment of General Surgery, The Fourth Affiliated Hospital of Anhui Medical University, Hefei, China.ORCID 0000-0003-3071-8788
Anhui Medical University · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is the most frequent digestive system malignant tumour and the second most common cause of cancer death globally. Cancer stem cell (CSC) is a small percentage of cancer cells in solid tumours that have differentiation, self-renewal and tumorigenic capabilities. They have an active participation in the initiation, development, metastasis, recurrence and resistance of tumours to chemotherapy and radiotherapy. Gastric cancer stem cells (GCSCs) have been shown to be correlated with GC initiation and metastasis. In this study, we found that TAK1 expression level in GC tissues was significantly increased compared to the adjacent non-cancerous tissues by RT-qPCR, Western blot and immunohistochemistry. TAK1 has been identified as a critical molecule that promoted a variety of malignant GC phenotypes both in vivo and in vitro and promoted the self-renewal of GCSCs. Mechanistically, TAK1 was up-regulated by IL-6 and prevented the degradation of yes-associated protein (YAP) in the cytoplasm by binding to YAP. Thus, TAK1 promoted the SOX2 and SOX9 transcription and the self-renewal and oncogenesis of GCSCs. Our findings provide insights into the mechanism of self-renewal and tumorigenesis of TAK1 in GCSCs and have broad implications for clinical therapies.

Indexed as

CarcinogenesisCell DifferentiationCell Line, TumorCell ProliferationCell Self RenewalGene Expression Regulation, NeoplasticHumansInterleukin-6MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNeoplastic Stem CellsSignal TransductionSOX9 Transcription FactorSOXB1 Transcription FactorsStomach NeoplasmsTransforming Growth Factor betaInterleukin-6MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesSOX2 protein, humanSOX9 protein, humanSOX9 Transcription FactorSOXB1 Transcription FactorsTransforming Growth Factor betaYAP1 protein, humanYAP-Signaling Proteinscancer stem cellsgastric cancerTGFβ-activated kinase 1YAP

Identifiers

PMID34075691
PMCPMC8278074
OpenAlexW3164474866

What OpenQuestion holds

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LicenceCC BY
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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.