Evidence map›Paper›PMID 29879092›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Cryptochrome 2 (CRY2) Suppresses Proliferation and Migration and Regulates Clock Gene Network in Osteosarcoma Cells.

Yueming Yu, Yinghua Li, Lei Zhou, Gong Yang, Minghai Wang, Yang Hong

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  8. Review
  9. c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024
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  15. Cancer, hear my battle CRY.Journal of pineal research · 2020
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  19. Monocarboxylate Transporter 4 (MCT4) Overexpression Is Correlated with Poor Prognosis of Osteosarcoma.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Yueming YuDepartment of Orthopedics, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Yinghua LiCentral Laboratory, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Lei ZhouDepartment of Orthopedics, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Gong YangCentral Laboratory, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Minghai WangDepartment of Orthopedics, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Yang HongDepartment of Orthopedics, Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China (mainland).
Obstetrics and Gynecology Hospital of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Circadian disruption is a potential cancer risk factor in humans. However, the role of the clock gene, cryptochrome 2 (CRY2), in osteosarcoma (OS) is still not clear. MATERIAL AND METHODS To evaluate the potential role of CRY2 in HOS osteosarcoma cells, CRY2-silenced cell lines were established. Furthermore, we investigated the effect of CRY2 knockdown on HOS cells by CCK-8, colony formation, migration assay, and flow cytometry, in vitro. RESULTS CRY2 knockdown promoted HOS OS cell proliferation and migration. We used a cell cycle assay to show that CRY2 knockdown increased the S phase cell population and reduced the G1 phase cell population. Western blot analyses showed that CRY2 knockdown decreased P53 expression and increased expression of c-myc and cyclin D1. Simultaneously, CRY2 knockdown increased the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, but did not change the phosphorylation of c-Jun N terminal kinase (JNK) and P38. CRY2 knockdown also increased the expression of matrix metalloproteinase (MMP)-2 and β-catenin, and increased OS cell proliferation and migration by inducing cell cycle progression and promoting mitogen-activated protein kinase (MAPK) and Wnt/β-catenin signaling pathways. Although it has previously been unclear whether the expression of CRY2 affects the expression of other clock genes in the clock gene network, our results show that knockdown of CRY2 significantly increased the mRNA expression of CRY1, Period (PER) 1, PER2, BMAL1, and CLOCK. CONCLUSIONS Our results suggest that CRY2 may be an anti-oncogene in OS, whose functions involve both downstream genes and other circadian genes.

Indexed as

Gene Regulatory Networksbeta CateninBiological ClocksCell CycleCell Line, TumorCell MovementCell ProliferationCryptochromeseIF-2 KinaseGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansOsteosarcomaRNA, MessengerWnt Signaling Pathwaybeta CateninCRY2 protein, humanCryptochromeseIF-2 KinaseRNA, Messenger

Identifiers

PMID29879092
PMCPMC6020744
OpenAlexW2807137765

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.