Evidence map›Paper›PMID 26960688›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

miR-522 contributes to cell proliferation of hepatocellular carcinoma by targeting DKK1 and SFRP2.

Hao Zhang, Chao Yu, Meiyuan Chen, Zhu Li, Se Tian, Jianxin Jiang, Chengyi Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Drug Discovery of DKK1 Inhibitors.Frontiers in pharmacology · 2022
    Review
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  18. The role of Dickkopf family in cancers: from Bench to Bedside.American journal of cancer research · 2017
    Review
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

7 authors at 2 institutions in 1 country.

Hao ZhangDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Chao YuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Meiyuan ChenDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Zhu LiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Se TianDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China.
Jianxin JiangDepartment of Hepatic-Biliary-Pancreatic Surgery, Hubei Cancer Hospital, 116 Zhuodaoquan south road, Hongshan district, Wuhan, 430079, Hubei, People's Republic of China. jjx731003@163.com.
Chengyi SunDepartment of Hepatobiliary Surgery, Affiliated Hospital of Guiyang Medical College, 28 Guiyi Street, Yunyan District, Guiyang, 550004, Guizhou, China. chengyisun2014@163.com.
Nanyang Medical College · CNHubei Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The morbidity and mortality of hepatocellular carcinoma (HCC) is very high, finding new therapeutic targets are critical for HCC treatment. miR-522 has been demonstrated to be upregulated in HCC tissues, but its role in HCC progression remains to be elucidated. In this report, we found miR-522 was upregulated in HCC cells and tissues, miR-522 overexpression promoted cell proliferation, colony formation, and cell cycle progression, whereas knockdown of miR-522 reduced these effects. We also analyzed the expression of several key cell cycle regulatory proteins and found overexpression of miR-522-inhibited cell cycle inhibitors p21 and p27 expression and enhanced cyclin D1 expression and the level of Rb phosphorylation, vice versa. These suggested miR-522-accelerated G1/S transition. DKK1 (dickkopf-1) and SFRP2 (secreted frizzled-related protein 2) were the targets of miR-522, their expression was inversely with miR-522 in HCC tissues. DKK1 and SFRP2 the antagonists of Wnt signaling, suggesting miR-522-promoted HCC progression through activating Wnt signaling. miR-522 might be a valuable target for HCC therapy.

Indexed as

Blotting, WesternCarcinoma, HepatocellularCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansIntercellular Signaling Peptides and ProteinsLiver NeoplasmsMembrane ProteinsMicroRNAsReverse Transcriptase Polymerase Chain ReactionSecreted Frizzled-Related ProteinsUp-RegulationDKK1 protein, humanIntercellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN522 microRNA, humanSecreted Frizzled-Related ProteinsSFRP2 protein, humanCell proliferationDKK1 and SFRP2HCCmiR-522

Identifiers

PMID26960688
OpenAlexW2296328793

What OpenQuestion holds

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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.