Evidence map›Paper›PMID 26790956›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Direct targeting sperm-associated antigen 9 by miR-141 influences hepatocellular carcinoma cell growth and metastasis via JNK pathway.

Guohua Lou, Xuejun Dong, Caixia Xia, Bingjue Ye, Qiuyue Yan, Shanshan Wu, Ye Yu, Feifei Liu, Min Zheng, Zhi Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 46 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

11 authors at 3 institutions in 1 country.

Guohua LouState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. louguohua@zju.edu.cn.
Xuejun DongShaoxing People's Hospital, Shaoxing Hospital, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. dxj9666@163.com.
Caixia XiaState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. 531865304@qq.com.
Bingjue YeState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. 529449496@qq.com.
Qiuyue YanShaoxing People's Hospital, Shaoxing Hospital, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. yanqiuyue2014@163.com.
Shanshan WuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. wushanshan08@aliyun.com.
Ye YuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. yuye177@163.com.
Feifei LiuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. liufeifei9009@163.com.
Min ZhengState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. charming_hz@163.com.
Zhi ChenState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. zjuchenzhi@zju.edu.cn.
Yanning LiuState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, 79# Qingchun Road, 6A-17, Hangzhou, 310003, China. liuyanning@zju.edu.cn.
State Key Laboratory of Diagnosis and Treatment of Infectious DiseasesZhejiang University · CNShaoxing People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aberrant expression of sperm-associated antigen 9 (SPAG9) is associated with numerous cancers, including hepatocellular carcinoma (HCC). The exploration of molecules and mechanisms regulating SPAG9 expression may provide new options for HCC therapy.

methodsMiRNA target prediction programs were used to explore SPAG9-targeted miRNAs. SPAG9 and miR-141 expression were detected in HCC tissues and cell lines by Western blot and real-time PCR. Dual-luciferase reporter assay was utilized to validate SPAG9 as a direct target gene of miR-141. Cell proliferation, invasion, and migration assays were used to determine whether miR-141-mediated regulation of SPAG9 could affect HCC progression.

resultsAn inverse correlation was observed between SPAG9 and miR-141 expression in HCC tissues and cell lines. Dual-luciferase reporter assay further showed that SPAG9 was a direct target gene of miR-141. The ectopic expression of miR-141 could markedly suppress SPAG9 expression in HCC cells. MiR-141 overexpression also resulted in significantly reduced cell proliferation, invasion, and migration, and imitation of the SPAG9 knockdown effects on HCC cells. Furthermore, SPAG9 restoration in miR-141-expressing cells sufficiently attenuated the tumor-suppressive effects of miR-141. Finally, JNK activity was found to be reduced by miR-141 overexpression the same way as by SPAG9 silencing. The overexpression of SPAG9 lacking its 3'-UTR significantly restored JNK activity and its downstream genes in miR-141-transfected HCC cells.

conclusionMiR-141 suppression may cause aberrant expression of SPAG9 and promote HCC tumorigenesis via JNK pathway.

Indexed as

3' Untranslated RegionsAdaptor Proteins, Signal TransducingCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMAP Kinase Signaling SystemMicroRNAsNeoplasm Metastasis3' Untranslated RegionsAdaptor Proteins, Signal TransducingMicroRNAsMIRN141 microRNA, humanSPAG9 protein, human

Identifiers

PMID26790956
PMCPMC4721207
OpenAlexW2280502662

What OpenQuestion holds

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LicenceCC BY
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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.