DNA

Part:BBa_K2440032

Designed by: Qijie Xu   Group: iGEM17_NUDT_CHINA   (2017-10-22)


miR-489 target sequence

It is the target sequence of miR-489, 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-489 in an Ago2 dependent manner, that is, knockdown of miR-489 was achieved by transfecting cells with miRNA locker.

MiR-489 was firstly found in the adult fish’s brain and eye.1

Compared to the corresponding non-tumor tissues, miR-489 was frequently downregulated in colorectal cancer (CRC). By Kaplan-Meier analysis, lower CRC recurrence free survival years in the group with elevated miR-489 expression than those with lower miR-489 expression. Moreover, miR-489 targets the 3'-UTR of the HDAC7 transcript and downregulates its expression, and HDAC7 expression promoted tumor cell proliferation and invasion. In conclusion, miR-489 suppresses tumor invasion and metastasis in CRC by targeting HDAC7.2

Moreover, miR-489 can inhibit proliferation, cell cycle progression and induces apoptosis of glioma cells via targeting SPIN1-mediated PI3K/AKT pathway.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.Cloning and expression of new microRNAs from zebrafish. Kloosterman WP, Steiner FA, Berezikov E, de Bruijn E, van de Belt J, Verheul M, Cuppen E, Plasterk RH Nucleic Acids Res. 34:2558-2569(2006).

2.MiR-489 suppresses tumor growth and invasion by targeting HDAC7 in colorectal cancer. Gao S, Liu H, Hou S, Wu L, Yang Z, Shen J, Zhou L, Zheng SS, Jiang B.

3.MiR-489 inhibits proliferation, cell cycle progression and induces apoptosis of glioma cells via targeting SPIN1-mediated PI3K/AKT pathway. Li Y, Ma X, Wang Y, Li G.

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