Evidence map›Paper›PMID 30103211›Full record

ArticleAging2018

Anillin is required for tumor growth and regulated by miR-15a/miR-16-1 in HBV-related hepatocellular carcinoma.

Yi-Fan Lian, Yan-Lin Huang, Jia-Liang Wang, Mei-Hai Deng, Tian-Liang Xia, Mu-Sheng Zeng, Min-Shan Chen, Hong-Bo Wang, Yue-Hua Huang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Cancers · 2024
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  14. NInternational journal of biological sciences · 2023
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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

9 authors at 2 institutions in 1 country.

Yi-Fan Lian *Guangdong Provincial Key Laboratory of Liver Disease Research, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yan-Lin Huang *Department of Infectious Diseases, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jia-Liang WangGuangdong Provincial Key Laboratory of Liver Disease Research, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Mei-Hai DengDepartment of Hepatobiliary Surgery, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Tian-Liang XiaState Key Laboratory of Southern China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Mu-Sheng ZengState Key Laboratory of Southern China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Min-Shan ChenDepartment of Hepatobiliary Surgery, Sun Yat-sen University Cancer Center, Guangzhou, China.
Hong-Bo WangGuangdong Provincial Key Laboratory of Liver Disease Research, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yue-Hua HuangGuangdong Provincial Key Laboratory of Liver Disease Research, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anillin (ANLN) is an actin-binding protein essential for assembly of cleavage furrow during cytokinesis. Although reportedly overexpressed in various human cancers, its role in hepatocellular carcinoma (HCC) is unclear. To address this issue, we confirmed that in 436 liver samples obtained from surgically removed HCC tissues, higher ANLN expression was detected in tumor tissues than in adjacent non-tumor tissues of HCC as measured by immunohistochemistry, quantitative real-time PCR and western blotting. Correlation and Kaplan-Meier analysis revealed that patients with higher ANLN expression were associated with worse clinical outcomes and a shorter survival time, respectively. Moreover, ANLN inhibition resulted in growth restraint, reduced colony formation, and a lower sphere number in suspension culture. Mechanistically, ANLN deficiency induced an increasing number of multinucleated cells along with the activation of apoptosis signaling and DNA damage checkpoints. Furthermore, HBV infection increased ANLN expression by inhibiting the expression of microRNA (miR)-15a and miR-16-1, both of which were identified as ANLN upstream repressors by targeting its 3' untranslated region. Thus, we conclude that ANLN promotes tumor growth by ways of decreased apoptosis and DNA damage. Expression level of ANLN significantly influences the survival probability of HCC patients and may represent a promising prognostic biomarker.

Indexed as

AdultAnimalsApoptosisCarcinoma, HepatocellularCell Line, TumorCell ProliferationCloning, MolecularContractile ProteinsDNA DamageFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHepatitis BHepatitis B virusHepatocytesHumansanillinContractile ProteinsMicroRNAsMirn15a microRNA, mouseMIRN15 microRNA, humanMIRN16 microRNA, humanRNA, MessengerANLNCell growthHepatocellular carcinomamicroRNAPrognostic biomarker

Identifiers

PMID30103211
PMCPMC6128427
OpenAlexW2886617908

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.