Abstract:
:MicroRNAs (miRs) have been demonstrated to be important in the establishment and progression of colon cancer. However the underlying molecular mechanisms remain to be fully elucidated. Polypeptide N‑acetylgalactosaminyltransferase4 (GALNT4) participates in numerous cellular processes, including tumorigenesis. The present study used reverse transcription‑quantitative polymerase chain reaction and western blotting to investigate the expression levels of miR‑4262 and GALNT4 in tissues and cells. In addition, MTS and colony formation assays, and cell cycle analysis were performed to evaluate the effect of miR‑4262 on cell proliferation and the cell cycle. The findings demonstrated that miR‑4262 was a direct target of GALNT4 mRNA. Overexpression of miR‑4262 was demonstrated to decrease GALNT4 mRNA and protein expression levels, and thereby suppressed cell viability, growth and cell‑cycle progression in SW480 and SW620 colon cancer cells. In addition, knockdown of miR‑4262 significantly increased the cell viability, growth, and cell‑cycle progression of SW480 and SW620 cells. The expression level of miR‑4262 was observed to be downregulated as the expression of GALNT4 was upregulated in colon cancer tissues and cell lines. In conclusion, the results demonstrated that miR‑4262 may be involved in the development of colon cancer via targeting of GALNT4. The miR‑4262/GALNT4 axis may be a novel target for diagnosing and understanding the underlying molecular mechanism of colon cancer.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Qu JJ,Qu XY,Zhou DZdoi
10.3892/mmr.2017.7057subject
Has Abstractpub_date
2017-10-01 00:00:00pages
3731-3736issue
4eissn
1791-2997issn
1791-3004journal_volume
16pub_type
杂志文章abstract::Advanced glycation end products (AGEs) are a contributing factor in the angiogenesis that is characteristic of proliferative diabetic retinopathy. However, a previous study made a promising observation that domain I‑IV of β2‑glycoprotein I (DI‑IV) inhibits angiogenesis in human umbilical vein cells. The present study ...
journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2014.2970
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abstract::Wnt/β-catenin signaling dysregulation is involved in tumorigenesis. Furthermore, epigenetic modification of the Dickkopf (DKK) family (DKK1‑4) has been shown to be important in the regulation of Wnt signaling. However, the functions and mechanism of DKK2 in the development and progression of prostate cancer remain unc...
journal_title:Molecular medicine reports
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doi:10.3892/mmr.2016.5502
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abstract::Toll-like receptors (TLRs) are critical in the induction of the immune response in tumor development. TLR7 has previously been demonstrated to be associated with the development of pancreatic cancer, and the release of cytokines and chemokines from other types of cancer cell; however, the specific expression induced b...
journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
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abstract::The authors of the above article wish to retract their paper. Subsequently to its publication, in addition to certain irreconcilable differences in opinion shared among the authors, they have realized that, in their analysis of the role of peroxisome proliferator‑activated receptor γ in brain microvascular endothelial...
journal_title:Molecular medicine reports
pub_type: 杂志文章,撤回出版物
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2018.9691
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2015.4554
更新日期:2016-01-01 00:00:00
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更新日期:2015-06-01 00:00:00
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2015.3370
更新日期:2015-07-01 00:00:00
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2018.8450
更新日期:2018-03-01 00:00:00
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2017.7697
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:10.3892/mmr.2016.6070
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
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journal_title:Molecular medicine reports
pub_type: 杂志文章
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journal_title:Molecular medicine reports
pub_type: 杂志文章
doi:
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