Evidence map›Paper›PMID 30246456›Full record

ArticleJournal of cellular and molecular medicine2018

Galectin-3 promotes CXCR2 to augment the stem-like property of renal cell carcinoma.

Chang-Shuo Huang, Shye-Jye Tang, Mei-Hsuan Lee, Chien-Chih Chang Wang, Guang-Huan Sun, Kuang-Hui Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 30% 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, 22 citations in OpenAlex.

  1. Review
  2. Galectin-3: action and clinical utility in chronic kidney disease.International urology and nephrology · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. FMNL1 Exhibits Pro-Metastatic ActivityFrontiers in oncology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

6 authors at 3 institutions in 1 country.

Chang-Shuo HuangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Shye-Jye TangInstitute of Marine Biotechnology, National Taiwan Ocean University, Keelung, Taiwan.
Mei-Hsuan LeeDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Chien-Chih Chang WangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Guang-Huan SunDivision of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Kuang-Hui SunDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.ORCID 0000-0001-8824-6416
National Yang Ming Chiao Tung University · TWNational Taiwan Ocean University · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although targeted therapy is usually the first-line treatment for advanced renal cell carcinoma (RCC), some patients can experience drug resistance. Cancer stem cells are tumour-initiating cells that play a vital role in drug resistance, metastasis and cancer relapse, while galectins (Gal) participate in tumour progression and drug resistance. However, the exact role of galectins in RCC stemness is yet unknown. In this study, we grew a subpopulation of RCC cells as tumour spheres with higher levels of stemness-related genes, such as Oct4, Sox2 and Nanog. Among the Gal family, Gal-3 in particular was highly expressed in RCC tumour spheres. To further investigate Gal-3's role in the stemness of RCC, lentivirus-mediated knockdown and overexpression of Gal-3 in RCC cells were used to examine both in vitro and in vivo tumorigenicity. We further assessed Gal-3 expression in RCC tissue microarray using immunohistochemistry. Upon suppressing Gal-3 in parental RCC cells, invasion, colony formation, sphere-forming ability, drug resistance and stemness-related gene expression were all significantly decreased. Furthermore, CXCL6, CXCL7 and CXCR2 were down-regulated in Gal-3-knockdown tumour spheres, while CXCR2 overexpression in Gal-3-knockdown RCC restored the ability of sphere formation. Gal-3 overexpression in RCC promoted both in vitro and in vivo tumorigenicity, and its expression was correlated with CXCR2 expression and tumour progression in clinical tissues. RCC patients with higher co-expressions of Gal-3 and CXCR2 demonstrated a worse survival rate. These results indicate that highly expressed Gal-3 may up-regulate CXCR2 to augment RCC stemness. Gal-3 may be a prognostic and innovative target of combined therapy for treating RCC.

Indexed as

AnimalsCarcinogenesisCarcinoma, Renal CellCell Line, TumorCell MovementCell Self RenewalChemokinesDisease ProgressionDown-RegulationDrug Resistance, NeoplasmGalectin 3HumansKidney NeoplasmsMaleMice, Inbred NODMice, SCIDChemokinesCXCR2 protein, humanGalectin 3Receptors, Interleukin-8Bcancer stem cellsCXCR2galectin-3renal cell carcinoma

Identifiers

PMID30246456
PMCPMC6237593
OpenAlexW2893522384

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.