Literature DB >> 25680556

Lentiviral DDX46 knockdown inhibits growth and induces apoptosis in human colorectal cancer cells.

Ming Li1, Yanchao Ma2, Pei Huang2, Aonan Du2, Xiaodong Yang3, Shuyu Zhang2, Chungen Xing3, Fenju Liu2, Jianping Cao2.   

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer related deaths worldwide. RNA helicases have been widely implicated in various types of cancer development. DDX46 belongs to the DEAD box family of RNA helicases, which are involved in the regulation of secondary RNA structures. The expression pattern of DDX46 in cancer tissues and the role of DDX46 in CRC progression have not been determined. In this study, we detected DDX46 protein expression in human CRC and adjacent tissues using immunohistochemistry. Our results showed that 87.04% of the columnar adenocarcinoma cases displayed high levels of focal nuclear DDX46 staining, and DDX46 protein expression was strongly increased in CRC tissues compared to adjacent tissues. Next, DDX46 RNAi lentivirus (DDX46-RNAi-LV) was used to silence the expression of DDX46 in the human colon carcinoma cells. Cells treated with the DDX46-RNAi-LV exhibited markedly reduced cell proliferation assessed by the MTT assay and visualized colony formation. Moreover, DDX46 silencing resulted in apoptotic induction via increased expression of cleaved caspase-3 and PARP. These results indicate that DDX46 is critical for CRC cell proliferation and is a potential therapeutic target for CRC treatment.
Copyright © 2015 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Colorectal cancer; DDX46; Lentivirus; Proliferation; RNAi

Mesh:

Substances:

Year:  2015        PMID: 25680556     DOI: 10.1016/j.gene.2015.02.020

Source DB:  PubMed          Journal:  Gene        ISSN: 0378-1119            Impact factor:   3.688


  12 in total

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3.  Hydroxylated-Graphene Quantum Dots Induce DNA Damage and Disrupt Microtubule Structure in Human Esophageal Epithelial Cells.

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9.  Silencing of DHX32 increases the proliferation of liver cancer cells.

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10.  Integrated Bioinformatics Analysis Reveals Marker Genes and Potential Therapeutic Targets for Pulmonary Arterial Hypertension.

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