Evidence map›Paper›PMID 35094008›Full record

ArticleOncogene2022

Hyperglycemia-induced oxidative stress promotes tumor metastasis by upregulating vWF expression in endothelial cells through the transcription factor GATA1.

Han-Seok Jeong, Da-Hye Lee, Seung-Hoon Kim, Chang-Han Lee, Hyun Mu Shin, Hang-Rae Kim, Chung-Hyun Cho

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  12. Diabetes and Cancer: A Twisted Bond.Oncology reviews · 2024
    Review
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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 at 1 institution in 4 countries.

Han-Seok JeongDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Da-Hye LeeDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Seung-Hoon KimDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Chang-Han LeeDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Hyun Mu ShinDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.ORCID http://orcid.org/0000-0002-4521-8391
Hang-Rae KimDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.ORCID http://orcid.org/0000-0002-3983-6193
Chung-Hyun ChoDepartment of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea. iamhyun@snu.ac.kr.ORCID http://orcid.org/0000-0002-0585-713X
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) characterized by hyperglycemia is a chronic metabolic disorder that leads to many symptoms and vascular complications. Despite the close association between DM and cancer progression, the response and role of endothelial cells (ECs) under diabetic conditions in tumor metastasis remain to be elucidated. In this study, we sought to determine whether and how ECs under diabetic conditions contribute to tumor metastasis. We have taken advantage of syngeneic mouse tumor models of Lewis lung carcinoma (LLC) and melanoma (B16F10) cells and a streptozotocin (STZ)-induced hyperglycemia model. We demonstrated that hyperglycemia increased the metastasis of LLC and B16F10 cells in an experimental metastasis model with an intravenous injection of the tumor cells. We also found that hyperglycemia promoted lung metastasis of tumor cells by increasing the adhesiveness of ECs to facilitate the adhesion of tumor cells to ECs rather than affecting the metastatic behavior of tumor cells themselves. From the analysis of gene expression in primary lung ECs from STZ-treated mice, we identified that vWF promoted the adhesion of tumor cells to ECs and the transendothelial migration of tumor cells. Mechanistically, hyperglycemia-induced oxidative stress in ECs, and increased oxidative stress enhanced vWF expression in ECs through an increase in the transcription factor GATA1. These results provide evidence for the role of vWF in ECs in promoting hyperglycemia-induced tumor metastasis and potential therapeutic targets for the regulation of vWF expression in ECs and hyperglycemia-induced tumor metastasis.

Indexed as

Carcinoma, Lewis LungDiabetes MellitusHyperglycemiaLung NeoplasmsAnimalsDisease Models, AnimalEndothelial CellsGATA1 Transcription FactorHumansMiceOxidative StressGATA1 protein, humanGATA1 Transcription Factor

Identifiers

PMID35094008
OpenAlexW4210607028

What OpenQuestion holds

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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.