Evidence map›Paper›PMID 33057010›Full record

ArticleCell death & disease2020

RASSF1A inhibits PDGFB-driven malignant phenotypes of nasopharyngeal carcinoma cells in a YAP1-dependent manner.

Ying-Ying Liang, Xu-Bin Deng, Xian-Tao Lin, Li-Li Jiang, Xiao-Ting Huang, Zhi-Wen Mo, Ya-Wei Yuan, Muy-Teck Teh

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

8 authors at 3 institutions in 2 countries.

Ying-Ying LiangDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Xu-Bin DengDepartment of Internal Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Xian-Tao LinDepartment of Internal Oncology, The First Affiliated Hospital of Hainan Medical University, Haiko, China.
Li-Li JiangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Science, Guangzhou Medical University, Guangzhou, China.
Xiao-Ting HuangDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Zhi-Wen MoDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Ya-Wei YuanDepartment of Radiation Oncology, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China.
Muy-Teck TehCancer Research Institute, Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China. m.t.teh@qmul.ac.uk.ORCID 0000-0002-7725-8355
Guangzhou Medical University · CNGuiyang Medical University · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a highly aggressive tumor characterized by distant metastasis. Deletion or down-regulation of the tumor suppressor protein ras-association domain family protein1 isoform A (RASSF1A) has been confirmed to be a key event in NPC progression; however, little is known about the effects or underlying mechanism of RASSF1A on the malignant phenotype. In the present study, we observed that RASSF1A expression inhibited the malignant phenotypes of NPC cells. Stable silencing of RASSF1A in NPC cell lines induced self-renewal properties and tumorigenicity in vivo/in vitro and the acquisition of an invasive phenotype in vitro. Mechanistically, RASSF1A inactivated Yes-associated Protein 1 (YAP1), a transcriptional coactivator, through actin remodeling, which further contributed to Platelet Derived Growth Factor Subunit B (PDGFB) transcription inhibition. Treatment with ectopic PDGFB partially increased the malignancy of NPC cells with transient knockdown of YAP1. Collectively, these findings suggest that RASSF1A inhibits malignant phenotypes by repressing PDGFB expression in a YAP1-dependent manner. PDGFB may serve as a potential interest of therapeutic regulators in patients with metastatic NPC.

Indexed as

Actin CytoskeletonAdaptor Proteins, Signal TransducingAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationGenes, Tumor SuppressorHeterograftsHumansMiceNasopharyngeal CarcinomaNasopharyngeal NeoplasmsPhenotypeProto-Oncogene Proteins c-sisSignal TransductionAdaptor Proteins, Signal TransducingBiomarkers, TumorProto-Oncogene Proteins c-sisRASSF1 protein, humanTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID33057010
PMCPMC7560678
OpenAlexW3093285284

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.