Evidence map›Paper›PMID 31375748›Full record

ArticleOncogene2019

Tumor-treating fields induce autophagy by blocking the Akt2/miR29b axis in glioblastoma cells.

Eun Ho Kim, Yunhui Jo, Sei Sai, Mung-Jin Park, Jeong-Yub Kim, Jin Su Kim, Yeon-Joo Lee, Jae-Min Cho, Seo-Young Kwak, Jeong-Hwa Baek and 4 more

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07383649 (Initial Safety Lead-in Followed by a Phase II Trial to Study Anti- HCMV Therapy in Breast Cancer Patients With Progressive Intracranial Metastases and CMV Infection), which is not on this map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
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.

NCT07383649 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Initial Safety Lead-in Followed by a Phase II Trial to Study Anti- HCMV Therapy in Breast Cancer Patients With Progressive Intracranial Metastases and CMV Infection (The Breast CMV Study)

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2026 to 2030Enrolled28ConditionsBrain Cancer Metastatic, CMV ViremiaArmsValganciclovir
3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The therapeutic efficacy and application prospects of tumor-treating fields (TTFields) in resolving malignant tumors of central nervous system.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Tumor-treating fields in cancer therapy: advances of cellular and molecular mechanisms.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Regulation of autophagy by non-coding RNAs in human glioblastoma.Medical oncology (Northwood, London, England) · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

14 authors at 3 institutions in 1 country.

Eun Ho KimDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Yunhui JoDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Sei SaiDepartment of Basic Medical Sciences for Radiation Damages, National Institute of Radiological Sciences, Chiba, Japan.
Mung-Jin ParkDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Jeong-Yub KimDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Jin Su KimDivision of RI-Convergence Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Yeon-Joo LeeDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.ORCID http://orcid.org/0000-0002-6605-8761
Jae-Min ChoDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Seo-Young KwakCenter for Theragnosis, Biomedical Research Institute, Korea Institute of Science and Technology, Seoul, 02792, Republic of Korea.
Jeong-Hwa BaekDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Youn Kyoung JeongRadiation Non-clinical Center, Division of Radiation Research Infrastructure Operation, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.
Jie-Young SongDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea.ORCID http://orcid.org/0000-0002-5769-3886
Myonggeun YoonDepartment of Bio-Convergence Engineering, Korea University, Seoul, 02842, Republic of Korea. radioyoon@korea.ac.kr.
Sang-Gu HwangDivision of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, 01812, Republic of Korea. sgh63@kcch.re.kr.
Korea Institute of Radiological and Medical Sciences · KRKorea University · KRKorea Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-treating fields (TTFs) - a type of electromagnetic field-based therapy using low-intensity electrical fields - has recently been characterized as a potential anticancer therapy for glioblastoma multiforme (GBM). However, the molecular mechanisms involved remain poorly understood. Our results show that the activation of autophagy contributes to the TTF-induced anti-GBM activity in vitro or in vivo and GBM patient stem cells or primary in vivo culture systems. TTF-treatment upregulated several autophagy-related genes (~2-fold) and induced cytomorphological changes. TTF-induced autophagy in GBM was associated with decreased Akt2 expression, not Akt1 or Akt3, via the mTOR/p70S6K pathway. An Affymetrix GeneChip miRNA 4.0 Array analysis revealed that TTFs altered the expression of many microRNAs (miRNAs). TTF-induced autophagy upregulated miR-29b, which subsequently suppressed the Akt signaling pathway. A luciferase reporter assay confirmed that TTFs induced miR-29b to target Akt2, negatively affecting Akt2 expression thereby triggering autophagy. TTF-induced autophagy suppressed tumor growth in GBM mouse models subjected to TTFs as determined by positron emission tomography and computed tomography (PET-CT). GBM patient stem cells and a primary in vivo culture system with high Akt2 levels also showed TTF-induced inhibition. Taken together, our results identified autophagy as a critical cell death pathway triggered by TTFs in GBM and indicate that TTF is a potential treatment option for GBM.

Indexed as

AnimalsApoptosisAutophagyBrain NeoplasmsCell Line, TumorCell ProliferationElectromagnetic FieldsGlioblastomaHumansMiceMicroRNAsNeoplastic Stem CellsProto-Oncogene Proteins c-aktSignal TransductionXenograft Model Antitumor AssaysAKT2 protein, humanMicroRNAsMIRN296 microRNA, humanProto-Oncogene Proteins c-akt

Identifiers

PMID31375748
OpenAlexW2964743865

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.