Abstract：
:Smarcd1 is a component of an evolutionary conserved chromatin remodeling complex-SWI/SNF, which is involved in transcription factor recruitment, DNA replication, recombination, and repair. Suppression of the SWI/SNF complex required for cellular differentiation and gene regulation may be inducible for cell proliferation and tumorigenicity. However, the inhibitory role of Smarcd1 in human glioblastoma cells has not been well illustrated. Both U87 and U251 human glioblastoma cell lines were employed in the present study. The lentivirus-mediated gene knockdown and overexpression approach was conducted to determine the function of Smarcd1. The protein levels were tested by western blot, and the relative mRNA contents were detected by quantitative real-time PCR. Cell viability was tested by CCK-8 and colony-forming assay. Transwell assays were utilized to evaluate the motility and invasive ability. Flow cytometry was employed to analyze cell cycle and apoptosis. SPSS software was used for statistical analysis. Low expression of Smarcd1 was observed in glioblastoma cell lines and in patients with high-grade glioma. Importantly, the depletion of Smarcd1 promoted cell proliferation, invasion, and chemoresistance, whereas enhanced expression of Smarcd1 inhibited tumor-malignant phenotypes. Mechanistic research demonstrated that overexpression of Smarcd1 decreased the expression of Notch1, while knockdown of Notch1 increased the expression of Smarcd1 through Hes1 suppression. Hence, the crosstalk between Smarcd1 and Notch1, which formed a feedback loop, was crucial in regulation of glioblastoma malignant phenotypes. Furthermore, targeting Smarcd1 could be a potential strategy for human glioblastoma treatment.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Zhu Y,Wang H,Fei M,Tang T,Niu W,Zhang Ldoi
10.1007/s12035-020-02190-zsubject
Has Abstractpub_date
2020-11-14 00:00:00eissn
0893-7648issn
1559-1182pii
10.1007/s12035-020-02190-zpub_type
杂志文章abstract：:Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease manifested by the progressive loss of upper and lower motoneurons. The pathomechanism of ALS is complex and not yet fully understood. Neuroinflammation is believed to significantly contribute to disease progression. Inflammasome activation was re...
journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-016-0322-4
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-018-1387-z
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-017-0695-z
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journal_title：Molecular neurobiology
pub_type： 杂志文章,评审
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pub_type： 杂志文章,评审
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pub_type： 杂志文章,评审
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journal_title：Molecular neurobiology
pub_type： 杂志文章,meta分析,评审
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更新日期：2015-12-01 00:00:00
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pub_type： 杂志文章,评审
doi：10.1007/BF02935639
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pub_type： 杂志文章,评审
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-016-0280-x
更新日期：2017-12-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-016-0144-4
更新日期：2017-10-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章,评审
doi：10.1007/BF02935629
更新日期：1989-10-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-019-01701-x
更新日期：2020-01-01 00:00:00
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更新日期：2020-05-01 00:00:00
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pub_type： 杂志文章,评审
doi：10.1007/BF02816114
更新日期：1994-08-01 00:00:00
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pub_type： 杂志文章
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pub_type： 杂志文章,评审
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pub_type： 杂志文章
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更新日期：2018-09-01 00:00:00
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pub_type： 杂志文章
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更新日期：2020-11-10 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
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journal_title：Molecular neurobiology
pub_type： 杂志文章,评审
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更新日期：2011-02-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-016-0187-6
更新日期：2017-11-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
doi：10.1007/s12035-014-9013-1
更新日期：2016-01-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章
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更新日期：2016-05-01 00:00:00
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journal_title：Molecular neurobiology
pub_type： 杂志文章,评审
doi：10.1385/MN:26:1:109
更新日期：2002-08-01 00:00:00
