RNA interference against Biot2, a novel mouse testis - specific gene, inhibits the growth of tumor cells

• Autorzy: Wang C -T , Zhang P. , Wang Y.-S. , Ruan X.-Z. , Li Z.-Y. , Peng F. , Yang H.-S. , Wei Y.-Q.
• Języki publikacji: EN

Abstrakty

EN

Biot2 is a novel murine testis-specific gene that was first identified using the SEREX technique, and named by our laboratory. Using conventional RT-PCR and real time RT-PCR, we tested the expression profile of Biot2 in normal tissues and various murine tumor cell lines. Using RNA interference, we studied the biological function of Biot2 in tumorigenesis. We applied various types of growth assay, such as the in vitro MTT, colony-forming and BrdU incorporation assays, along with in vivo tumorigenicity assays, to reveal its inhibition of tumor cell proliferation. The results revealed that the Biot2 transcript was detected only and strongly in the testis tissues and abundantly in five types of murine cancer cell line. Treating B16 murine melanoma, LL/2 murine Lewis lung carcinoma and CT26 murine colorectal adenocarcinoma with special shRNA targeting Biot2 can significantly reduce the proliferation rate of these three tumor cell lines in vitro, as measured by the MTT, colony-forming and BrdU incorporation assays. The tumorigenicity of the CT26 cells transfected with special shRNA targeting Biot2 was also decreased distinctly in vivo compared with the control. It was therefore concluded that Biot2 plays a key role in tumorigenesis and could be a potential target for biotherapy.

Słowa kluczowe

EN

RNA interference; Biot2 gene; mouse; mice; murine gene; specific gene; cell growth; tumour cell; tumourigenesis; tumour cell line; proliferation

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 2009
• Tom: 14
• Numer: 3
• Opis fizyczny: p.363-376,fig.,ref.

Twórcy

autor

Wang C -T

• Sichuan University, Keyuan Road 4, Chengdu, Sichuan, 610041, P.R.China

autor

Zhang P.

autor

Wang Y.-S.

autor

Ruan X.-Z.

autor

Li Z.-Y.

autor

Peng F.

autor

Yang H.-S.

autor

Wei Y.-Q.

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