Evidence map›Paper›PMID 34681583›Full record

ArticleInternational journal of molecular sciences2021

K-RAS Acts as a Critical Regulator of CD44 to Promote the Invasiveness and Stemness of GBM in Response to Ionizing Radiation.

Yi Zhao, Jae-Hyeok Kang, Ki-Chun Yoo, Seok-Gu Kang, Hae-June Lee, Su-Jae Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  7. The Role of RAS in CNS Tumors: A Key Player or an Overlooked Oncogene?International journal of molecular sciences · 2025
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  18. The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor.International journal of molecular sciences · 2022
    Review
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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

6 authors at 3 institutions in 1 country.

Yi ZhaoDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea.ORCID 0000-0002-6668-9889
Jae-Hyeok KangDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea.
Ki-Chun YooDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea.
Seok-Gu KangDepartment of Neurosurgery, Brain Tumor Center, Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Korea.
Hae-June LeeDivision of Radiation Effect, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Korea.
Su-Jae LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea.
Hanyang University · KRKorea Institute of Radiological and Medical Sciences · KRYonsei University · KR

Funding

National Research Foundation of Korea No.2019R1A2C2087551National Research Foundation of Korea No.2020M2C8A2069347
6 · The paper itself

Abstract

Radiation therapy is a current standard-of-care treatment and is used widely for GBM patients. However, radiation therapy still remains a significant barrier to getting a successful outcome due to the therapeutic resistance and tumor recurrence. Understanding the underlying mechanisms of this resistance and recurrence would provide an efficient approach for improving the therapy for GBM treatment. Here, we identified a regulatory mechanism of CD44 which induces infiltration and mesenchymal shift of GBM. Ionizing radiation (IR)-induced K-RAS/ERK signaling activation elevates CD44 expression through downregulation of miR-202 and miR-185 expression. High expression of CD44 promotes SRC activation to induce cancer stemness and EMT features of GBM cells. In this study, we demonstrate that the K-RAS/ERK/CD44 axis is a key mechanism in regulating mesenchymal shift of GBM cells after irradiation. These findings suggest that blocking the K-RAS activation or CD44 expression could provide an efficient way for GBM treatment.

Indexed as

Radiation, IonizingBrain NeoplasmsCell Line, TumorCell MovementDown-RegulationExtracellular Signal-Regulated MAP KinasesGlioblastomaHumansHyaluronan ReceptorsKaplan-Meier EstimateMicroRNAsProto-Oncogene Proteins p21(ras)RNA InterferenceRNA, Small InterferingSignal TransductionCD44 protein, humanExtracellular Signal-Regulated MAP KinasesHyaluronan ReceptorsKRAS protein, humanMicroRNAsMIRN202 microRNA, humanProto-Oncogene Proteins p21(ras)RNA, Small InterferingCD44glioblastoma (GBM)ionizing radiation (IR)K-RAS

Identifiers

PMID34681583
PMCPMC8539357
OpenAlexW3205951060

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.