Evidence map›Paper›PMID 33168027›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and activating VEGFR-2 signaling pathway in hepatocellular carcinoma.

Fei Teng, Ju-Xiang Zhang, Qi-Meng Chang, Xu-Bo Wu, Wei-Guo Tang, Jian-Fa Wang, Jin-Feng Feng, Zi-Ping Zhang, Zhi-Qiu Hu

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 154 citations in OpenAlex.

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  11. Identification of apoptosisZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  12. GABPA-Mediated Expression of HPN-AS1 Facilitates Cell Apoptosis and Inhibits Cell Proliferation in Hepatocellular Carcinoma by Promoting eIF4A3 Degradation.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
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  19. Role of miR-424 in the carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
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15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Fei Teng *Department of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Ju-Xiang Zhang *Shanghai Med-X Engineering Center for Medical Equipment and Technology, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Qi-Meng ChangDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Xu-Bo WuDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Wei-Guo TangDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Jian-Fa WangDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Jin-Feng FengDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China.
Zi-Ping ZhangDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China. zhang_zp@fudan.edu.cn.
Zhi-Qiu HuDepartment of Hepatobiliary and Pancreatic Surgery, Minhang Hospital, Fudan University, Shanghai, 201199, People's Republic of China. huzq@fudan.edu.cn.ORCID http://orcid.org/0000-0002-3244-1607
Fudan University · CNShanghai Jiao Tong University · CN

Funding

Fundamental Medical Project of Minhang Hospital of Fudan University Project Foundation 2019MHJC04Shanghai Minhang Science and Technology Commission (CN) 2019MHZ079
6 · The paper itself

Abstract

backgroundLong non-coding RNAs (lncRNAs) are crucial in the invasion, angiogenesis, progression, and metastasis of hepatocellular carcinoma (HCC). The lncRNA MYLK-AS1 promotes the growth and invasion of HCC through the EGFR/HER2-ERK1/2 signaling pathway. However, the clinical significance of MYLK-AS1 in HCC still needs to be further determined.

methodsBioinformatic analysis was performed to determine the potential relationship among MYLK-AS1, miRNAs and mRNAs. A total of 156 samples of normal liver and paired HCC tissues from HCC patients were used to evaluate MYLK-AS1 expression by qRT-PCR. Human HCC cell lines were used to evaluate the colony formation, cell proliferation, migration, invasion, cell cycle and apoptosis after transfection of lentiviral short-hairpin RNAs (shRNAs) targeting MYLK-AS1 or MYLK-AS1 vectors. The competitive endogenous RNA (ceRNA) mechanism was clarified using fluorescence in situ hybridization (FISH), Western blotting, qPCR, RNA binding protein immunoprecipitation (RIP), and dual luciferase reporter analysis.

resultsMYLK-AS1 up-regulation was detected in the HCC tumor tissues and cell lines associated with the enhancement of the angiogenesis and tumor progression. The down-regulation of MYLK-AS1 reversed the effects on angiogenesis, proliferation, invasion and metastasis in the HCC cells and in vivo. MYLK-AS1 acted as ceRNA, capable of regulating the angiogenesis in HCC, while the microRNA miR-424-5p was the direct target of MYLK-AS1. Promoting the angiogenesis and the tumor proliferation, the complex MYLK-AS1/miR-424-5p activated the VEGFR-2 signaling through E2F7, whereas the specific targeting of E2F transcription factor 7 (E2F7) by miR-424-5p, was indicated by the mechanism studies.

conclusionsMYLK-AS1 and E2F7 are closely related to some malignant clinicopathological features and prognosis of HCC, thus the MYLK-AS1/ miR-424-5p/E2F7 signaling pathway might represent a promising treatment strategy to combat HCC.

Indexed as

Calcium-Binding ProteinsCarcinoma, HepatocellularDisease ProgressionE2F7 Transcription FactorFemaleHumansLiver NeoplasmsMaleMicroRNAsMiddle AgedMyosin-Light-Chain KinaseNeovascularization, PathologicPrognosisRNA, AntisenseRNA, Long NoncodingSignal TransductionCalcium-Binding ProteinsE2F7 protein, humanE2F7 Transcription FactorMicroRNAsMIRN424 microrna, humanMYLK protein, humanMyosin-Light-Chain KinaseRNA, AntisenseRNA, Long NoncodingVascular Endothelial Growth Factor Receptor-2Competing endogenous RNAE2F7Hepatocellular carcinomaLong non-coding RNAs, MYLK-AS1VEGFR-2, miR-424-5p

Identifiers

PMID33168027
PMCPMC7650167
OpenAlexW3105388559

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.