Limits...
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 decreased the growth of glioma cells. (A, B) U87 and U251 cells were seeded into 96-well plates and cultured for 0 hours, 24 hours, 48 hours, 72 hours and 96 hours respectively, MTT assay was employed to detect the effect of MALAT1 knockdown on cell growth at different time points in both cells. The glioma cells transfected with Scramble was used as the negative control. *P < 0.05 vs. the control. (C, D) U87 and U251 cells in serum-free medium were placed into the upper transwell chamber, the invasion assays in vitro were carried out to detect the effect of MALAT1 knockdown on cell invasion after 24 hours of incubation. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4835592&req=5

Figure 2: Knockdown of MALAT1 decreased the growth of glioma cells. (A, B) U87 and U251 cells were seeded into 96-well plates and cultured for 0 hours, 24 hours, 48 hours, 72 hours and 96 hours respectively, MTT assay was employed to detect the effect of MALAT1 knockdown on cell growth at different time points in both cells. The glioma cells transfected with Scramble was used as the negative control. *P < 0.05 vs. the control. (C, D) U87 and U251 cells in serum-free medium were placed into the upper transwell chamber, the invasion assays in vitro were carried out to detect the effect of MALAT1 knockdown on cell invasion after 24 hours of incubation. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control.

Mentions: As indicated that MALAT1 could be effectively knocked down, cell growth was then detected via MTT assay. Glioma cells generally manifest powerful growth ability, which, however, was greatly attenuated with knockdown of MALAT1 in a time dependent manner, especially at 72 hours and 96 hours post transfection of MALAT1 siRNA (Fig. 2A and 2B). Next, we studied if MALAT1 knockdown would also affect cell invasion in glioma cell lines. We found that both U87 and U251 cells displayed reduced cell mobility after MALAT1 knockdown (Fig. 2C and 2D).


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 decreased the growth of glioma cells. (A, B) U87 and U251 cells were seeded into 96-well plates and cultured for 0 hours, 24 hours, 48 hours, 72 hours and 96 hours respectively, MTT assay was employed to detect the effect of MALAT1 knockdown on cell growth at different time points in both cells. The glioma cells transfected with Scramble was used as the negative control. *P < 0.05 vs. the control. (C, D) U87 and U251 cells in serum-free medium were placed into the upper transwell chamber, the invasion assays in vitro were carried out to detect the effect of MALAT1 knockdown on cell invasion after 24 hours of incubation. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Knockdown of MALAT1 decreased the growth of glioma cells. (A, B) U87 and U251 cells were seeded into 96-well plates and cultured for 0 hours, 24 hours, 48 hours, 72 hours and 96 hours respectively, MTT assay was employed to detect the effect of MALAT1 knockdown on cell growth at different time points in both cells. The glioma cells transfected with Scramble was used as the negative control. *P < 0.05 vs. the control. (C, D) U87 and U251 cells in serum-free medium were placed into the upper transwell chamber, the invasion assays in vitro were carried out to detect the effect of MALAT1 knockdown on cell invasion after 24 hours of incubation. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control.
Mentions: As indicated that MALAT1 could be effectively knocked down, cell growth was then detected via MTT assay. Glioma cells generally manifest powerful growth ability, which, however, was greatly attenuated with knockdown of MALAT1 in a time dependent manner, especially at 72 hours and 96 hours post transfection of MALAT1 siRNA (Fig. 2A and 2B). Next, we studied if MALAT1 knockdown would also affect cell invasion in glioma cell lines. We found that both U87 and U251 cells displayed reduced cell mobility after MALAT1 knockdown (Fig. 2C and 2D).

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