Evidence map›Paper›PMID 37099250›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

Aberrant expression of circular RNA DHPR facilitates tumor growth and metastasis by regulating the RASGEF1B/RAS/MAPK axis in hepatocellular carcinoma.

Zeyi Guo, Qingyu Xie, Yanping Wu, Haiyu Mo, Jiajun Zhang, Guolin He, Zhongzhe Li, Luxiang Gan, Lei Feng, Ting Li and 8 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

18 authors at 3 institutions in 1 country.

Zeyi GuoDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Qingyu XieDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Yanping WuDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Haiyu MoDepartment of Medical Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510000, P. R. China.
Jiajun ZhangDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Guolin HeDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Zhongzhe LiDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Luxiang GanDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Lei FengDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Ting LiDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Yi WangDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Yu FuDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Lei CaiDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Shao LiDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China.
Chao YuDepartment of General Surgery, Zhujiang hospital, Southern Medical University, Guangzhou, 510000, P. R. China.
Yi GaoDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China. gaoyi@smu.edu.cn.
Mingxin PanDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China. pmxwxy@sohu.com.
Shunjun FuDepartment of Hepatobiliary Surgery II, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510000, P. R. China. fsj103@163.com.
Zhujiang Hospital · CNSouthern Medical University · CNSun Yat-sen University Cancer Center · CN

Funding

National Natural Science Foundation of China 31972926National Natural Science Foundation of China 82072627Natural Science Foundation of Guangdong Province 2021B1515230011Natural Science Foundation of Guangdong Province 2023A1515010141
6 · The paper itself

Abstract

backgroundCircular RNAs (circRNAs) are noncoding RNAs. Accumulating evidence suggests that circRNAs play a critical role in human biological processes, especially tumorigenesis, and development. However, the exact mechanisms of action of circRNAs in hepatocellular carcinoma (HCC) remain unclear.

methodsBioinformatic tools and RT-qPCR were used to identify the role of circDHPR, a circRNA derived from the dihydropteridine reductase (DHPR) locus, in HCC and para-carcinoma tissues. Kaplan-Meier analysis and the Cox proportional hazard model were used to analyze the correlation between circDHPR expression and patient prognosis. Lentiviral vectors were used to establish stable circDHPR-overexpressing cells. In vitro and in vivo studies have shown that tumor proliferation and metastasis are affected by circDHPR. Mechanistic assays, including Western blotting, immunohistochemistry, dual-luciferase reporter assays, fluorescence in situ hybridization, and RNA immunoprecipitation, have demonstrated the molecular mechanism underlying circDHPR.

resultsCircDHPR was downregulated in HCC, and low circDHPR expression was associated with poor overall survival and disease-free survival rates. CircDHPR overexpression inhibits tumor growth and metastasis in vitro and in vivo. Further systematic studies revealed that circDHPR binds to miR-3194-5p, an upstream regulator of RASGEF1B. This endogenous competition suppresses the silencing effect of miR-3194-5p. We confirmed that circDHPR overexpression inhibited HCC growth and metastasis by sponging miR-3194-5p to upregulate the expression of RASGEF1B, which is regarded as a suppressor of the Ras/MAPK signaling pathway.

conclusionsAberrant circDHPR expression leads to uncontrolled cell proliferation, tumorigenesis, and metastasis. CircDHPR may serve as a biomarker and therapeutic target for HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMicroRNAsCarcinogenesisCell Line, TumorCell ProliferationDihydropteridine ReductaseGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceRNA, CircularDihydropteridine ReductaseMicroRNAsRNA, CircularCircular RNADHPRHepatocellular carcinomaRASGEF1BRas/MAPK

Identifiers

PMID37099250
PMCPMC12974678
OpenAlexW4367047566

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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.