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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

MALAT1 was highly expressed in glioma patients and cell lines. (A) 37 glioma tissue samples and adjacent normal brain samples were selected, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in glioma patients. The adjacent normal brain tissues (paracancer group) were used as the negative control. (B) Human malignant glioma cell lines U87 and U251 cells were cultured, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in both cells. The normal glia cell line NHA was used as the negative control. (C) U87 and U251 cells were transfected with siRNA targeting MALAT1, QRT-PCR assay was employed to detect the endogenous expression of MALAT1 to confirm the knockdown efficiency. The glioma 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 1: MALAT1 was highly expressed in glioma patients and cell lines. (A) 37 glioma tissue samples and adjacent normal brain samples were selected, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in glioma patients. The adjacent normal brain tissues (paracancer group) were used as the negative control. (B) Human malignant glioma cell lines U87 and U251 cells were cultured, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in both cells. The normal glia cell line NHA was used as the negative control. (C) U87 and U251 cells were transfected with siRNA targeting MALAT1, QRT-PCR assay was employed to detect the endogenous expression of MALAT1 to confirm the knockdown efficiency. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.

Mentions: The relative expression level of MALAT1 in glioma patients were examined with qRT-PCR assay, and the level of MALAT1 in glioma samples were compared to that in adjacent normal brain tissues. The result showed that the expression of MALAT1 was significantly increased in cancerous tissues compared with that in paracancerous tissues (Fig. 1A). Meanwhile, the expression of MALAT1 in U87 and U251 cells were also verified via qRT-PCR assay, and the expression of MALAT1 was also greatly up-regulated in these two malignant glioma cell lines when compared with that in the normal human astrocytes (NHA) cell line (Fig. 1B). To further explore the function of MALAT1 in glioma growth, U87 and U251 cells were transfected with siRNA targeting MALAT1. The endogenous expression of MALAT1 was effectively knocked down (Fig. 1C).


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)

MALAT1 was highly expressed in glioma patients and cell lines. (A) 37 glioma tissue samples and adjacent normal brain samples were selected, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in glioma patients. The adjacent normal brain tissues (paracancer group) were used as the negative control. (B) Human malignant glioma cell lines U87 and U251 cells were cultured, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in both cells. The normal glia cell line NHA was used as the negative control. (C) U87 and U251 cells were transfected with siRNA targeting MALAT1, QRT-PCR assay was employed to detect the endogenous expression of MALAT1 to confirm the knockdown efficiency. The glioma 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 1: MALAT1 was highly expressed in glioma patients and cell lines. (A) 37 glioma tissue samples and adjacent normal brain samples were selected, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in glioma patients. The adjacent normal brain tissues (paracancer group) were used as the negative control. (B) Human malignant glioma cell lines U87 and U251 cells were cultured, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in both cells. The normal glia cell line NHA was used as the negative control. (C) U87 and U251 cells were transfected with siRNA targeting MALAT1, QRT-PCR assay was employed to detect the endogenous expression of MALAT1 to confirm the knockdown efficiency. The glioma cells transfected with Scramble was used as the negative control.*P < 0.05 vs. the control; †P < 0.01 vs. the control.
Mentions: The relative expression level of MALAT1 in glioma patients were examined with qRT-PCR assay, and the level of MALAT1 in glioma samples were compared to that in adjacent normal brain tissues. The result showed that the expression of MALAT1 was significantly increased in cancerous tissues compared with that in paracancerous tissues (Fig. 1A). Meanwhile, the expression of MALAT1 in U87 and U251 cells were also verified via qRT-PCR assay, and the expression of MALAT1 was also greatly up-regulated in these two malignant glioma cell lines when compared with that in the normal human astrocytes (NHA) cell line (Fig. 1B). To further explore the function of MALAT1 in glioma growth, U87 and U251 cells were transfected with siRNA targeting MALAT1. The endogenous expression of MALAT1 was effectively knocked down (Fig. 1C).

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