Evidence map›Paper›PMID 31636512›Full record

ArticleCancer cell international2019

Histone methyltransferase SUV39H2 regulates cell growth and chemosensitivity in glioma via regulation of hedgehog signaling.

Ran Wang, Lilin Cheng, Xi Yang, Xin Chen, Yifeng Miao, Yongming Qiu, Zhiyi Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  11. [Curcumol reverses temozolomide resistance in glioma cells by regulating the UTX/MGMT axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 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

7 authors at 2 institutions in 1 country.

Ran WangDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lilin ChengDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xi YangDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xin ChenDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yifeng MiaoDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yongming QiuDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Zhiyi ZhouDepartment of Neurosurgery, South Campus, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Renji Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMalignant glioma is one of the essentially incurable tumors with chemoresistance and tumor recurrence. As a histone methyltransferase, SUV39H2 can trimethylate H3K9. SUV39H2 is highly expressed in many types of human tumors, while the function of SUV39H2 in the development and progression of glioma has never been elucidated.

methodsRT-qPCR and IHC were used to test SUV39H2 levels in glioma tissues and paired normal tissues. The clinical relevance of SUV39H2 in glioma was analyzed in a public database. Colony formation assays, CCK-8 assays, and flow cytometry were conducted to explore the role of SUV39H2 in the growth of glioma cells in vitro. A cell line-derived xenograft model was applied to explore SUV39H2's role in U251 cell proliferation in vivo. Sphere formation assays, RT-qPCR, flow cytometry, and IF were conducted to illustrate the role of SUV39H2 in the stemness and chemosensitivity of glioma. Luciferase reporter assays and WB were applied to determine the function of SUV39H2 in Hh signaling.

resultsSUV39H2 was highly expressed in glioma tissues relative to normal tissues. SUV39H2 knockdown inhibited cell proliferation and stemness and promoted the chemosensitivity of glioma cells in vitro. In addition, SUV39H2 knockdown also significantly inhibited glioma cell growth in vivo. Moreover, we further uncovered that SUV39H2 regulated hedgehog signaling by repressing HHIP expression.

conclusionsOur findings delineate the role of SUV39H2 in glioma cell growth and chemosensitivity as a pivotal regulator of the hedgehog signaling pathway and may support SUV39H2 as a potential target for diagnosis and therapy in glioma management.

Indexed as

Cancer stem cellGliomaHHIPHh signalingSUV39H2

Identifiers

PMID31636512
PMCPMC6794832
OpenAlexW2980851527

What OpenQuestion holds

Textmetadata
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.