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Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
Journal of Korean Medical Science ; : 688-694, 2016.
Article in English | WPRIM | ID: wpr-195412
ABSTRACT
The metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) is a highly conserved long non-coding RNA (lncRNA) gene. However, little is known about the pathological role of lncRNA MALAT1 in glioma. In the present study, we explored the expression level of lncRNA MALAT1 in primary glioma tissues as well as in U87 and U251 glioma cell lines. Using qRT-PCR, we found that the expression of lncRNA MALAT1 was significantly increased in glioma tissues compared with that of paracancerous tissues. Meanwhile, the expression of MALAT1 was highly expressed in U98 and U251 cells. In order to explore the function of MALAT1, the expression of MALAT1 was greatly reduced in U87 and U251 cells transfected with siRNA specifically targeting MALAT1. Consequently, cell viability of U87 and U251 cells were drastically decreased after the knockdown of MALAT1. Concomitantly, the apoptosis rate of the two cell lines was dramatically increased. Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC. In summary, the current study indicated a promoting role of MALAT1 in the development of glioma cell.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Biomarkers, Tumor / Down-Regulation / Cell Movement / Blotting, Western / Proto-Oncogene Proteins c-myc / Apoptosis / Cyclin D1 / RNA, Small Interfering / RNA Interference / Cell Line, Tumor Limits: Humans Language: English Journal: Journal of Korean Medical Science Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Biomarkers, Tumor / Down-Regulation / Cell Movement / Blotting, Western / Proto-Oncogene Proteins c-myc / Apoptosis / Cyclin D1 / RNA, Small Interfering / RNA Interference / Cell Line, Tumor Limits: Humans Language: English Journal: Journal of Korean Medical Science Year: 2016 Type: Article