Difference between revisions of "Part:BBa K2440020"
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MiRNA locker assembled by using this modularized DNA part was able to bind miR-184 in an Ago2 dependent manner, that is, knockdown of miR-184 was achieved by transfecting cells with miRNA locker.
 
MiRNA locker assembled by using this modularized DNA part was able to bind miR-184 in an Ago2 dependent manner, that is, knockdown of miR-184 was achieved by transfecting cells with miRNA locker.
 +
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Hsa-miR-184 was firstly found in mouse eyes. And it is aslo identified by BLAST searching of a cloned miRNA in another species (Homo sapiens; Mus musculus; Fugu rubripes ; Danio rerio; Drosophila melanogaster).<sup>1</sup>
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In vitro functional studies demonstrated that miR-184 significantly inhibited colorectal cancer cell proliferation, migration and invasion. Notably, insulin-like growth factor 1 receptor (IGF-1R) was identified as a direct target of miR-184 in colorectal cancer. Furthermore, the functions of IGF-1R small interfering RNA were similar to those induced by miR-184 in colorectal cancer, suggesting IGF-1R as a functional target of miR-184 in colorectal cancer. So miR-184 may be a novel therapeutic strategy regimen of targeted therapy for colorectal cancer.<sup>2</sup>
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Moreover, miR-184 can inhibit proliferation and promotes apoptosis of human colon cancer SW480 and HCT116 cells by downregulating C-MYC and BCL-2.<sup>3</sup>
  
 
===Sequence and Features===
 
===Sequence and Features===
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This part is sequenced as correct after construction.
 
This part is sequenced as correct after construction.
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==Reference==
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1.New microRNAs from mouse and human. Lagos-Quintana M, Rauhut R, Meyer J, Borkhardt A, Tuschl T RNA. 9:175-179(2003).
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2.MicroRNA-184 inhibits cell proliferation and metastasis in human colorectal cancer by directly targeting IGF-1R. Wu G, Liu J, Wu Z, Wu X, Yao X.
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3.MicroRNA-184 inhibits proliferation and promotes apoptosis of human colon cancer SW480 and HCT116 cells by downregulating C-MYC and BCL-2. Wang YB, Zhao XH, Li G, Zheng JH, Qiu W.

Latest revision as of 01:02, 1 November 2017


miR-184 target sequence

It is the target sequence of miR-184, a modularized DNA part from a set of chemically synthetic oligo DNA library.

Usage and Biology

MiRNA locker assembled by using this modularized DNA part was able to bind miR-184 in an Ago2 dependent manner, that is, knockdown of miR-184 was achieved by transfecting cells with miRNA locker.

Hsa-miR-184 was firstly found in mouse eyes. And it is aslo identified by BLAST searching of a cloned miRNA in another species (Homo sapiens; Mus musculus; Fugu rubripes ; Danio rerio; Drosophila melanogaster).1

In vitro functional studies demonstrated that miR-184 significantly inhibited colorectal cancer cell proliferation, migration and invasion. Notably, insulin-like growth factor 1 receptor (IGF-1R) was identified as a direct target of miR-184 in colorectal cancer. Furthermore, the functions of IGF-1R small interfering RNA were similar to those induced by miR-184 in colorectal cancer, suggesting IGF-1R as a functional target of miR-184 in colorectal cancer. So miR-184 may be a novel therapeutic strategy regimen of targeted therapy for colorectal cancer.2

Moreover, miR-184 can inhibit proliferation and promotes apoptosis of human colon cancer SW480 and HCT116 cells by downregulating C-MYC and BCL-2.3

Sequence and Features

Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]


Experimental Validation

This part is sequenced as correct after construction.


Reference

1.New microRNAs from mouse and human. Lagos-Quintana M, Rauhut R, Meyer J, Borkhardt A, Tuschl T RNA. 9:175-179(2003).

2.MicroRNA-184 inhibits cell proliferation and metastasis in human colorectal cancer by directly targeting IGF-1R. Wu G, Liu J, Wu Z, Wu X, Yao X.

3.MicroRNA-184 inhibits proliferation and promotes apoptosis of human colon cancer SW480 and HCT116 cells by downregulating C-MYC and BCL-2. Wang YB, Zhao XH, Li G, Zheng JH, Qiu W.