Evidence map›Paper›PMID 35706810›Full record

ArticleTranslational cancer research2022

Mechanism of HBV-positive liver cancer cell exosomal miR-142-3p by inducing ferroptosis of M1 macrophages to promote liver cancer progression.

Zongqiang Hu, Hui Zhang, Wei Liu, Yanfeng Yin, Jie Jiang, Chuntao Yan, Yiting Wang, Li Li

Open access · diamondAbstract read
In one paragraph

Article in Translational cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Ferroptosis in liver biology and diseases.Hepatology communications · 2026
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  13. Exosome is a Fancy Mobile Sower of Ferroptosis.Journal of cardiovascular translational research · 2024
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  19. The role of ferroptosis-related non-coding RNA in liver fibrosis.Frontiers in cell and developmental biology · 2024
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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

8 authors at 2 institutions in 1 country.

Zongqiang Hu *Department of Hepato-Pancreato-Biliary Surgery, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
Hui Zhang *Department of Hepato-Pancreato-Biliary Surgery, The People's Hospital of Chuxiong Yi Autonomous Prefecture & The Fourth Affiliated Hospital of Dali University, Chuxiong, China.
Wei Liu *Department of Hepato-Pancreato-Biliary Surgery, The People's Hospital of Chuxiong Yi Autonomous Prefecture & The Fourth Affiliated Hospital of Dali University, Chuxiong, China.
Yanfeng YinDepartment of Hepato-Pancreato-Biliary Surgery, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
Jie JiangDepartment of Hepato-Pancreato-Biliary Surgery, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
Chuntao YanThe Central Laboratory of Kunming First People's Hospital, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
Yiting WangThe Central Laboratory of Kunming First People's Hospital, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
Li LiDepartment of Hepato-Pancreato-Biliary Surgery, First People's Hospital of Kunming City & The Calmette Affiliated Hospital of Kunming Medical University, Kunming, China.
The First Hospital of Kunming · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Exosomes are becoming an important mediator of the interaction between tumor cells and the microenvironment. Ferroptosis is a newly discovered type of cell death. However, its role in the progression of liver cancer is largely unknown. The aim of the presents study was to analyze the mechanism by which hepatitis B virus (HBV)-positive liver cancer secretes exosomes to mediate the iron death of M1 macrophages, thereby promoting the development of liver cancer. Methods: Liver cancer tissues and peripheral blood with positive and negative clinical HBV infection were collected, and M-type macrophages, miR-142-3p, and recombinant solute carrier family 3, member 2 ( Results: The expression of miR-142-3p significantly increased in the exosomes extracted from the peripheral blood of patients with HBV-positive liver cancer. Genes related to intracellular iron metabolism and homeostasis, such as ferritin heavy chain 1 (FTH1), transferrin receptor 1 (TfR1), recombinant glutathione peroxidase 4 (GPX4), and activating transcription factor 4 (ATF4), had abnormal expression levels in M1 macrophages. HBV-positive HCC exosomes treated with M1-type macrophages had a weakened inhibitory effect on the invasion of HCC cells, but ferroptosis inhibitors could reverse the effect of HBV-positive HCC exosomes treated M1-type macrophages on HCC cells. Knockdown of the expression of miR-142-3p can also weaken the invasive ability of liver cancer cells. Conclusions: The results of the present study confirmed that HBV-positive liver cancer cell exosomal miR-142-3p can promote the progression of liver cancer by inducing iron death of M1-type macrophages.

Indexed as

ferroptosishepatitis B virus (HBV)liver cancerM1-type macrophagesmiR-142-3p

Identifiers

PMID35706810
PMCPMC9189167
OpenAlexW4283031287

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.