Evidence map›Paper›PMID 30420967›Full record

ArticleBioMed research international2018

Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway.

Wen Song, Zhenling Wang, Pengcheng Kan, Zhuolin Ma, Yaru Wang, Qiaoli Wu, Xiuhua Yao, Biao Zhang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 20 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

8 authors at 2 institutions in 1 country.

Wen SongThe Graduate School, Tianjin Medical University, Tianjin 300070, China.
Zhenling WangTianjin Neurosurgery Institute, Tianjin Cerebral Vascular and Neural Degenerative Disease Key Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, China.
Pengcheng KanThe Graduate School, Tianjin Medical University, Tianjin 300070, China.
Zhuolin MaThe Graduate School, Tianjin Medical University, Tianjin 300070, China.
Yaru WangThe Graduate School, Tianjin Medical University, Tianjin 300070, China.
Qiaoli WuTianjin Neurosurgery Institute, Tianjin Cerebral Vascular and Neural Degenerative Disease Key Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, China.
Xiuhua YaoTianjin Neurosurgery Institute, Tianjin Cerebral Vascular and Neural Degenerative Disease Key Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, China.
Biao ZhangTianjin Neurosurgery Institute, Tianjin Cerebral Vascular and Neural Degenerative Disease Key Laboratory, Tianjin Huanhu Hospital, Tianjin 300350, China.ORCID 0000-0002-9738-1123
Tianjin Huanhu Hospital · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers. This study was to detect the expression of BCL6 and its biological effect on glioma.

methodsRT-PCR and Western blot were used to detect the expression of BCL6 mRNA and protein in tissues and glioblastoma cell lines. The expression of BCL6 was knockdown in two glioblastoma cell lines (U87 and U251) using BCL6 shRNA. The CCK8, colony-formation, flow cytometry, Transwell, and wound-healing assays were used to evaluate the malignant phenotypic change of glioblastoma cells.

resultsThe expression of BCL6 was higher in glioma tissues and glioblastoma cell lines than normal tissues. Knockdown of BCL6 expression reduced the proliferation, migration, and invasion of glioblastoma cells. Moreover, knockdown of BCL6 changed expression of proteins related to malignant behaviors of glioblastoma cells. The suppression of BCL6 could increase chemosensitivity of U87 and U251 to temozolomide. Downregulation of BCL6 levels suppressed the expression of BCL2, cyclin D1, MMP2, and MMP9 proteins as well as two classic signaling pathway proteins p-AKT and p-ERK. Simultaneously, BAX and p21 protein levels were upregulated along with knockdown of BCL6.

conclusionsOur results indicated that BCL6 may be a tumor oncogene involved in the progression of glioma via affecting AKT and MAPK signaling pathways.

Indexed as

Antineoplastic AgentsBrainBrain NeoplasmsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Knockdown TechniquesGlioblastomaHumansPhenotypeProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-6Signal TransductionTemozolomideAntineoplastic AgentsBCL6 protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-6Temozolomide

Identifiers

PMID30420967
PMCPMC6211201
OpenAlexW2896645424

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.