Evidence map›Paper›PMID 30651129›Full record

ArticleBreast cancer research : BCR2019

Hydrodynamic shear stress promotes epithelial-mesenchymal transition by downregulating ERK and GSK3β activities.

Hye Yeon Choi, Gwang-Mo Yang, Ahmed Abdal Dayem, Subbroto Kumar Saha, Kyeongseok Kim, Youngbum Yoo, Kwonho Hong, Jin-Hoi Kim, Cassian Yee, Kyung-Mi Lee and 1 more

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Circulating Tumor Cells for the Monitoring of Lung Cancer Therapies.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. The Rise of Mechanobiology for Advanced Cell Engineering and Manufacturing.Advanced materials (Deerfield Beach, Fla.) · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Molecular Underpinnings of Brain Metastases.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Mechanical signatures in cancer metastasis.npj biological physics and mechanics · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 2 countries.

Hye Yeon ChoiDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Gwang-Mo YangDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Ahmed Abdal DayemDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Subbroto Kumar SahaDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Kyeongseok KimDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Youngbum YooDepartment of Surgery, Konkuk University School of Medicine, Seoul, 05030, Republic of Korea.
Kwonho HongDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Jin-Hoi KimDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea.
Cassian YeeDepartment of Melanoma Medical Oncology, MD Anderson Cancer Center, Houston, TX, 77054, USA.
Kyung-Mi LeeDepartment of Biochemistry and Molecular Biology, Korea University College of Medicine, 26-1 Anam-dong, Sungbuk-gu, Seoul, 02841, Republic of Korea. kyunglee@korea.ac.kr.
Ssang-Goo ChoDepartment of Stem Cell & Regenerative Biotechnology and Incurable Disease Animal Model and Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, Republic of Korea. ssangoo@konkuk.ac.kr.ORCID 0000-0002-0968-7932
Konkuk University · KRKorea University · KRThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-mesenchymal transition (EMT) occurs in the tumor microenvironment and presents an important mechanism of tumor cell intravasation, stemness acquisition, and metastasis. During metastasis, tumor cells enter the circulation to gain access to distant tissues, but how this fluid microenvironment influences cancer cell biology is poorly understood. METHODS AND

resultsHere, we present both in vivo and in vitro evidence that EMT-like transition also occurs in circulating tumor cells (CTCs) as a result of hydrodynamic shear stress (+SS), which promotes conversion of CD24

conclusionFluid shear stress experienced during systemic circulation of human breast tumor cells can lead to specific acquisition of mesenchymal stem cell (MSC)-like potential that promotes EMT, mesenchymal-epithelial transition, and metastasis to distant organs. Our data revealed that biomechanical forces appeared to be important microenvironmental factors that not only drive hematopoietic development but also lead to acquisition of CSLCs/TIC potential in cancer metastasis. Our data highlight that +SS is a critical factor that promotes the conversion of CTCs into distinct TICs in blood circulation by endowing plasticity to these cells and by maintaining their self-renewal signaling pathways.

Indexed as

AdultAgedAnimalsBreastBreast NeoplasmsCell Self RenewalEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesFemaleGlycogen Synthase Kinase 3 betaHEK293 CellsHumansHydrodynamicsMiceMiddle AgedNeoplasm InvasivenessExtracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3 betaGSK3B protein, humanEMT/METERK-GSK3βHydrodynamic shear stressROS/NOTumor-initiating cells

Identifiers

PMID30651129
PMCPMC6335853
OpenAlexW2913487628

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.