Evidence map›Paper›PMID 27626163›Full record

ArticleOncotarget2016

Galectin-3 supports stemness in ovarian cancer stem cells by activation of the Notch1 intracellular domain.

Hyeok Gu Kang, Da-Hyun Kim, Seok-Jun Kim, Yunhee Cho, Junghyun Jung, Wonhee Jang, Kyung-Hee Chun

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Targeting ovarian cancer stem cells: a new way out.Stem cell research & therapy · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. The Involvement of Alarmins in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Redox signaling by glutathione peroxidase 2 links vascular modulation to metabolic plasticity of breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Article
  15. Critical appraisal of epigenetic regulation of galectins in cancer.International journal of clinical oncology · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

7 authors.

Hyeok Gu KangDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Da-Hyun KimDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Seok-Jun KimDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Yunhee ChoDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Junghyun JungDepartment of Life Science, Dongguk University, Seoul, Republic of Korea.
Wonhee JangDepartment of Life Science, Dongguk University, Seoul, Republic of Korea.
Kyung-Hee ChunDepartment of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the most lethal gynecologic disease because usually, it is lately sensed, easily acquires chemoresistance, and has a high recurrence rate. Recent studies suggest that ovarian cancer stem cells (CSCs) are involved in these malignancies. Here, we demonstrated that galectin-3 maintains ovarian CSCs by activating the Notch1 intracellular domain (NICD1). The number and size of ovarian CSCs decreased in the absence of galectin-3, and overexpression of galectin-3 increased them. Overexpression of galectin-3 increased the resistance for cisplatin and paclitaxel-induced cell death. Silencing of galectin-3 decreased the migration and invasion of ovarian cancer cells, and overexpression of galectin-3 reversed these effects. The Notch signaling pathway was strongly activated by galectin-3 overexpression in A2780 cells. Silencing of galectin-3 reduced the levels of cleaved NICD1 and expression of the Notch target genes, Hes1 and Hey1. Overexpression of galectin-3 induced NICD1 cleavage and increased expression of Hes1 and Hey1. Moreover, overexpression of galectin-3 increased the nuclear translocation of NICD1. Interestingly, the carbohydrate recognition domain of galectin-3 interacted with NICD1. Overexpression of galectin-3 increased tumor burden in A2780 ovarian cancer xenografted mice. Increased expression of galectin-3 was detected in advanced stages, compared to stage 1 or 2 in ovarian cancer patients, suggesting that galectin-3 supports stemness of these cells. Based on these results, we suggest that targeting galectin-3 may be a potent approach for improving ovarian cancer therapy.

Indexed as

AnimalsApoptosisBlood ProteinsCell Line, TumorCell MovementCell ProliferationFemaleGalectin 3GalectinsGene Expression Regulation, NeoplasticHumansMice, NudeNeoplastic Stem CellsOvarian NeoplasmsReceptor, Notch1RNA InterferenceBlood ProteinsGalectin 3GalectinsLGALS3 protein, humanReceptor, Notch1cancer stem cellsgalectin-3Notch1ovarian cancer

Identifiers

PMID27626163
PMCPMC5356551

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LicenceCC BY
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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.