Evidence map›Paper›PMID 31508283›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2019

Genome-Wide CRISPR-Cas9 Screening Identifies NF-κB/E2F6 Responsible for EGFRvIII-Associated Temozolomide Resistance in Glioblastoma.

Kai Huang, Xing Liu, Yansheng Li, Qixue Wang, Junhu Zhou, Yunfei Wang, Feng Dong, Chao Yang, Zhiyan Sun, Chuan Fang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Review
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  7. Review
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  9. Article
  10. LTF regulates glioblastoma progression and temozolomide resistance via the NF-κB signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Versatile function of NF-ĸB in inflammation and cancer.Experimental hematology & oncology · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. Unlocking Glioblastoma Vulnerabilities with CRISPR-Based Genetic Screening.International journal of molecular sciences · 2024
    Review
  20. 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

15 authors at 4 institutions in 2 countries.

Kai HuangTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Xing LiuBeijing Neurosurgical Institute Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China.
Yansheng LiTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Qixue WangTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Junhu ZhouTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Yunfei WangTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Feng DongDepartment of Cell Biology 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics Tianjin Key Laboratory of Medical Epigenetics Tianjin Medical University Tianjin 300070 China.
Chao YangTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Zhiyan SunBeijing Neurosurgical Institute Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China.
Chuan FangDepartment of Neurosurgery Affiliated Hospital of Hebei University Baoding 071000 China.
Chaoyong LiuTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.
Yanli TanDepartment of Pathology Affiliated Hospital of Hebei University Baoding 071000 China.
Xudong WuDepartment of Cell Biology 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics Tianjin Key Laboratory of Medical Epigenetics Tianjin Medical University Tianjin 300070 China.
Tao JiangBeijing Neurosurgical Institute Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China.
Chunsheng KangTianjin Neurological Institute Key Laboratory of Post-Neurotrauma Neuro-Repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City Tianjin 300052 China.ORCID https://orcid.org/0000-0002-3255-3369
Tianjin Medical University General Hospital · CNCapital Medical University · CNAffiliated Hospital of Hebei University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amplification of epidermal growth factor receptor (EGFR) and active mutant EGFRvIII occurs frequently in glioblastoma (GBM) and contributes to chemo/radio-resistance in various cancers, especially in GBM. Elucidating the underlying molecular mechanism of temozolomide (TMZ) resistance in GBM could benefit cancer patients. A genome-wide screening under a clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 library is conducted to identify the genes that confer resistance to TMZ in EGFRvIII-expressing GBM cells. Deep sgRNA sequencing reveals 191 candidate genes that are responsible for TMZ resistance in EGFRvIII-expressing GBM cells. Notably, E2F6 is proven to drive a TMZ resistance, and E2F6 expression is controlled by the EGFRvIII/AKT/NF-κB pathway. Furthermore, E2F6 is shown as a promising therapeutic target for TMZ resistance in orthotopic GBM cell line xenografts and GBM patient-derived xenografts models. After integrating clinical data with paired primary-recurrent RNA sequencing data from 134 GBM patients who received TMZ treatment after surgery, it has been revealed that the E2F6 expression level is a predictive marker for TMZ response. Therefore, the inhibition of E2F6 is a promising strategy to conquer TMZ resistance in GBM.

Indexed as

CRISPR‐Cas9 librariesE2F6glioblastoma (GBM)temozolomide (TMZ) resistance

Identifiers

PMID31508283
PMCPMC6724471
OpenAlexW2964040556

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.