Evidence map›Paper›PMID 33397392›Full record

ArticleCancer cell international2021

Leptin Receptor (LEPR) promotes proliferation, migration, and invasion and inhibits apoptosis in hepatocellular carcinoma by regulating ANXA7.

He Huang, Jun Zhang, Fei Ling, Yuhong Huang, Min Yang, Yao Zhang, Yuanyi Wei, Qingqing Zhang, Honghai Wang, Lin Song and 3 more

Abstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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  6. Metabolic dysfunction-associated fatty liver disease and osteoporosis: the mechanisms and roles of adiposity.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 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

13 authors.

He HuangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Jun ZhangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Fei LingDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Yuhong HuangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Min YangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Yao ZhangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Yuanyi WeiDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Qingqing ZhangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Honghai WangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Lin SongHelen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94158, USA.
Ying WuDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Jiayu YangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China.
Jianwu TangDepartment of Pathology, College of Basic Medical Sciences, Dalian Medical University, 9 W. Lushun South Road, Dalian, 116044, Liaoning, China. Jwtang_53@sina.cn.

Funding

National Natural Science Foundation of China No.81071725
6 · The paper itself

Abstract

backgroundLeptin Receptor (LEPR) has been suggested to have several roles in cancer metastasis. However, the role of LEPR and its underlying mechanisms in lymphatic metastasis of hepatocarcinoma have not yet been studied.

methodsWe performed bioinformatics analysis, qRT-PCR, western blotting, immunohistochemistry, immunofluorescence, enzyme-linked immunosorbent, coimmunoprecipitation assays and a series of functional assays to investigate the roles of LEPR in hepatocellular carcinoma.

resultsWe discovered that LEPR was highly expressed in liver cancer tissues, and the expression of LEPR in Hca-F cells was higher than that in Hca-P cells. Furthermore, LEPR promotes the proliferation, migration and invasion and inhibits the apoptosis of hepatocarcinoma lymphatic metastatic cells. Further studies indicated that LEPR interacts with ANXA7. Mechanistically, LEPR regulated ERK1/2 and JAK2/STAT3 expression via ANXA7 regulation.

conclusionsThese findings unveiled a previously unappreciated role of LEPR in the regulation of lymphatic metastatic hepatocellular carcinoma, assigning ANXA7-LEPR as a promising therapeutic target for liver cancer treatments.

Indexed as

ANXA7apoptosiscell migrationcell proliferationhepatocellular carcinomainteracting proteinsLEPR

Identifiers

PMID33397392
PMCPMC7784271

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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.