Evidence map›Paper›PMID 37982952›Full record

ArticleHepatology international2024

Transferrin receptor 1 promotes hepatocellular carcinoma progression and metastasis by activating the mTOR signaling pathway.

Fu Wang, Wei-Qi Xu, Wan-Qin Zhang, Ru-Chen Xu, Jia-Lei Sun, Guang-Cong Zhang, Zhi-Yong Liu, Zhuo-Ran Qi, Ling Dong, Shu-Qiang Weng and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Hepatology international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  3. The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

14 authors at 2 institutions in 1 country.

Fu Wang *Department of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Wei-Qi Xu *Department of Hepatic Surgery, Shanghai Cancer Center, Fudan University, Shanghai, China.
Wan-Qin Zhang *Department of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Ru-Chen XuDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Jia-Lei SunDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Guang-Cong ZhangDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Zhi-Yong LiuDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Zhuo-Ran QiDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Ling DongDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Shu-Qiang WengDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Xi-Zhong ShenDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Tao-Tao LiuDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
Ying FangDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China. fang.ying@zs-hospital.sh.cn.
Ji-Min ZhuDepartment of Gastroenterology and Hepatology and Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China. zhu.jimin@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0002-2150-473X
Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

National Natural Science Foundation of China 81970505National Natural Science Foundation of China 82173122Natural Science Foundation of Shanghai 19ZR1434700Natural Science Foundation of Shanghai 22ZR1411800
6 · The paper itself

Abstract

backgroundAberrant iron metabolism is commonly observed in multiple tumor types, including hepatocellular carcinoma (HCC). However, as the key regulator of iron metabolism involved in iron absorption, the role of transferrin receptor (TFRC) in HCC remains elusive.

methodsThe mRNA and protein expression of TFRC were evaluated in paired HCC and adjacent non-tumor specimens. The correlation between TFRC level and clinicopathological features or prognostic significance was also analyzed. The role of TFRC on biological functions was finally studied in vitro and in vivo.

resultsThe TFRC level was remarkably upregulated in HCC tissues compared to paired peritumor tissues. Overexpressed TFRC positively correlated with serum alpha-fetoprotein, carcinoembryonic antigen, and poor tumor differentiation. Multivariate analysis demonstrated that upregulated TFRC was an independent predictive marker for poorer overall survival and disease-free survival in HCC patients. Loss of TFRC markedly impaired cell proliferation and migration in vitro and notably suppressed HCC growth and metastasis in vivo, while overexpression of TFRC performed an opposite effect. Mechanistically, the mTOR signaling pathway was downregulated with TFRC knockdown, and the mTOR agonist MHY1485 completely reversed the biological inhibition in HCC cells caused by TFRC knockdown. Furthermore, exogenous ferric citrate (FAC) or iron chelator reversed the changed biological functions and signaling pathway expression of HCC cells caused by TFRC knockdown or overexpression, respectively.

conclusionsOur study indicates that TFRC exerts an oncogenic role in HCC and may become a promising therapeutic target to restrain HCC progression.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIronReceptors, TransferrinSignal TransductionTOR Serine-Threonine KinasesIronMTOR protein, humanReceptors, TransferrinTOR Serine-Threonine KinasesCD71FK506-binding protein 12-rapamycin-associated protein 1HCCIron metabolismLiver cancerMammalian target of rapamycinTFRCTumor progression

Identifiers

PMID37982952
OpenAlexW4388829149

What OpenQuestion holds

Textmetadata
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.