Difference between revisions of "Part:BBa K2440018"

(Usage and Biology)
(Usage and Biology)
Line 9: Line 9:
 
MiRNA locker assembled by using this modularized DNA part was able to bind miR-384 in an Ago2 dependent manner, that is, knockdown of miR-384 was achieved by transfecting cells with miRNA locker.
 
MiRNA locker assembled by using this modularized DNA part was able to bind miR-384 in an Ago2 dependent manner, that is, knockdown of miR-384 was achieved by transfecting cells with miRNA locker.
  
Hsa-miR-384 was firstly found in human and rat.1
+
Hsa-miR-384 was firstly found in human and rat.<sup>1</sup>
  
MiR-384 was significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. The overexpression of miR-384 repressed the growth and invasion of NSCLC cells, whereas its suppression showed the opposite effect. Moreover, astrocyte elevated gene-1 (AEG-1) was identified as a target gene of miR-384. The overexpression of miR-384 significantly decreased AEG-1 expression and Wnt signaling, whereas its suppression promoted this pathway. Furthermore, miR-384 was inversely correlated with AEG-1 expression in NSCLC tissues. Additionally, restoration of AEG-1 expression in miR-384-overexpressing cells significantly reversed the antitumor effects of miR-3842.  
+
MiR-384 was significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. The overexpression of miR-384 repressed the growth and invasion of NSCLC cells, whereas its suppression showed the opposite effect. Moreover, astrocyte elevated gene-1 (AEG-1) was identified as a target gene of miR-384. The overexpression of miR-384 significantly decreased AEG-1 expression and Wnt signaling, whereas its suppression promoted this pathway. Furthermore, miR-384 was inversely correlated with AEG-1 expression in NSCLC tissues. Additionally, restoration of AEG-1 expression in miR-384-overexpressing cells significantly reversed the antitumor effects of miR-384. <sup>2</sup>
  
Moreover, miR-384 suppresses the growth and invasion of Renal Cell Carcinoma Cells (RCC) via downregulation of AEG-1, providing a potential therapeutic target for treatment of RCC3.
+
Moreover, miR-384 suppresses the growth and invasion of Renal Cell Carcinoma Cells (RCC) via downregulation of AEG-1, providing a potential therapeutic target for treatment of RCC.<sup>3</sup>
  
 
===Sequence and Features===
 
===Sequence and Features===

Revision as of 00:57, 1 November 2017


miR-384 target sequence

It is the target sequence of miR-384, 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-384 in an Ago2 dependent manner, that is, knockdown of miR-384 was achieved by transfecting cells with miRNA locker.

Hsa-miR-384 was firstly found in human and rat.1

MiR-384 was significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. The overexpression of miR-384 repressed the growth and invasion of NSCLC cells, whereas its suppression showed the opposite effect. Moreover, astrocyte elevated gene-1 (AEG-1) was identified as a target gene of miR-384. The overexpression of miR-384 significantly decreased AEG-1 expression and Wnt signaling, whereas its suppression promoted this pathway. Furthermore, miR-384 was inversely correlated with AEG-1 expression in NSCLC tissues. Additionally, restoration of AEG-1 expression in miR-384-overexpressing cells significantly reversed the antitumor effects of miR-384. 2

Moreover, miR-384 suppresses the growth and invasion of Renal Cell Carcinoma Cells (RCC) via downregulation of AEG-1, providing a potential therapeutic target for treatment of RCC.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.