Evidence map›Paper›PMID 36107262›Full record

ArticleCellular and molecular life sciences : CMLS2022

PHLDA1 promotes glioblastoma cell growth via sustaining the activation state of Ras.

Jiutao Wang, Ning Yao, Yamei Hu, Mingjuan Lei, Meixian Wang, Lu Yang, Satyananda Patel, Xiang Li, Kangdong Liu, Zigang Dong

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Jiutao WangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Ning YaoDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Yamei HuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Mingjuan LeiDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Meixian WangChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan, China.
Lu YangDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Satyananda PatelChina-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan, China.
Xiang LiDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Kangdong LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. kdliu@zzu.edu.cn.
Zigang DongDepartment of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China. dongzg@zzu.edu.cn.ORCID http://orcid.org/0000-0002-4174-4028
Zhengzhou University · CNChina-US (Henan) Hormel Cancer Institute · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 82073075Natural Science Foundation of Henan Province 162300410336
6 · The paper itself

Abstract

Activation of the Ras signaling pathway promotes the growth of malignant human glioblastoma multiforme (GBM). Mutations in Ras are rare in GBM, elevated levels of activated Ras are prevalently observed in GBM. However, the potential mechanism of how Ras is activated in GBM remains unclear. In this study, we screened a new interacted protein of Ras, PHLDA1. Our findings confirmed that PHLDA1 acted as an oncogene and promoted glioma progression and recurrence. We demonstrated that PHLDA1 was upregulated in GBM tissues and cells. PHLDA1 overexpression promoted cell proliferation and tumor growth. In terms of mechanism, PHLDA1 promoted cell proliferation by regulating Ras/Raf/Mek/Erk signaling pathway. Moreover, Src promotes GTPase activity of Ras via tyrosine 32 phosphorylation. PHLDA1 and Src competed for binding with Ras, inhibiting Ras phosphorylation by Src and rescuing Ras activity. This study may provide a new idea of the molecular mechanism underlying glioma progression and a novel potential therapeutic target for comprehensive glioblastoma treatment.

Indexed as

GlioblastomaCell ProliferationGTP PhosphohydrolasesHumansMitogen-Activated Protein Kinase KinasesTranscription FactorsTyrosineGTP PhosphohydrolasesMitogen-Activated Protein Kinase KinasesPHLDA1 protein, humanTranscription FactorsTyrosineGlioblastoma multiformePHLDA1RasRas phosphorylationSrc

Identifiers

PMID36107262
PMCPMC11803017
OpenAlexW4295908478

What Socratic 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 Socratic graph.