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Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells.

Xiang J, Guo S, Jiang S, Xu Y, Li J, Li L, Xiang J - J. Korean Med. Sci. (2016)

Bottom Line: 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.Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Yishui Central Hospital, Shandong, China .

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.

No MeSH data available.


Related in: MedlinePlus

Knockdown of MALAT1 increased the apoptosis rate of glioma cells. (A, B) U87 and U251 cells were seeded in 6 well plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. Annexin V-FITC/PI double staining assay was employed to detect the effect of MALAT1 knockdown on the apoptosis rate in U87 (A) and U251 (B) cells. The glioma cells transfected with Scramble was used as the negative control. FL2-H, FL2-Height.
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Figure 3: Knockdown of MALAT1 increased the apoptosis rate of glioma cells. (A, B) U87 and U251 cells were seeded in 6 well plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. Annexin V-FITC/PI double staining assay was employed to detect the effect of MALAT1 knockdown on the apoptosis rate in U87 (A) and U251 (B) cells. The glioma cells transfected with Scramble was used as the negative control. FL2-H, FL2-Height.

Mentions: We further examined the effect of MALAT1 knockdown on the apoptosis rate of glioma cells, which was determined by Annexin V-FITC/PI double staining assay. The results indicated that U87 and U251 cells transfected with siRNA targeting MALAT1 showed a much higher apoptosis rate than the cells with scramble siRNA (Fig. 3A and 3B).


Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells.

Xiang J, Guo S, Jiang S, Xu Y, Li J, Li L, Xiang J - J. Korean Med. Sci. (2016)

Knockdown of MALAT1 increased the apoptosis rate of glioma cells. (A, B) U87 and U251 cells were seeded in 6 well plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. Annexin V-FITC/PI double staining assay was employed to detect the effect of MALAT1 knockdown on the apoptosis rate in U87 (A) and U251 (B) cells. The glioma cells transfected with Scramble was used as the negative control. FL2-H, FL2-Height.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4835592&req=5

Figure 3: Knockdown of MALAT1 increased the apoptosis rate of glioma cells. (A, B) U87 and U251 cells were seeded in 6 well plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. Annexin V-FITC/PI double staining assay was employed to detect the effect of MALAT1 knockdown on the apoptosis rate in U87 (A) and U251 (B) cells. The glioma cells transfected with Scramble was used as the negative control. FL2-H, FL2-Height.
Mentions: We further examined the effect of MALAT1 knockdown on the apoptosis rate of glioma cells, which was determined by Annexin V-FITC/PI double staining assay. The results indicated that U87 and U251 cells transfected with siRNA targeting MALAT1 showed a much higher apoptosis rate than the cells with scramble siRNA (Fig. 3A and 3B).

Bottom Line: 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.Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Yishui Central Hospital, Shandong, China .

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.

No MeSH data available.


Related in: MedlinePlus