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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

CCND1 and MYC was down-regulated with MALAT1 knockdown. U87 and U251 cells were seeded in 60 mm plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. QRT-PCR and western blot analysis were employed to verify the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown in U87 cells (A, B) and U251 cells (C, D). The cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.
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Figure 4: CCND1 and MYC was down-regulated with MALAT1 knockdown. U87 and U251 cells were seeded in 60 mm plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. QRT-PCR and western blot analysis were employed to verify the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown in U87 cells (A, B) and U251 cells (C, D). The cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.

Mentions: It was reported that oncogenic genes CCND1 (21) and MYC (22) was expressed at high levels in glioma cells. We thus examined the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown via qRT-PCR and western blot analysis. The results showed that the expression of these two proteins were remarkably inhibited in both U87 (Fig. 4A and 4B) and U251 (Fig. 4C and 4D) glioma cells transfected with siRNA targeting MALAT1.


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)

CCND1 and MYC was down-regulated with MALAT1 knockdown. U87 and U251 cells were seeded in 60 mm plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. QRT-PCR and western blot analysis were employed to verify the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown in U87 cells (A, B) and U251 cells (C, D). The cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: CCND1 and MYC was down-regulated with MALAT1 knockdown. U87 and U251 cells were seeded in 60 mm plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. QRT-PCR and western blot analysis were employed to verify the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown in U87 cells (A, B) and U251 cells (C, D). The cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.
Mentions: It was reported that oncogenic genes CCND1 (21) and MYC (22) was expressed at high levels in glioma cells. We thus examined the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown via qRT-PCR and western blot analysis. The results showed that the expression of these two proteins were remarkably inhibited in both U87 (Fig. 4A and 4B) and U251 (Fig. 4C and 4D) glioma cells transfected with siRNA targeting MALAT1.

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