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Metastasis-associated lung adenocarcinoma transcript 1 promotes the proliferation of chondrosarcoma cell via activating Notch-1 signaling pathway.

Xu F, Zhang ZQ, Fang YC, Li XL, Sun Y, Xiong CZ, Yan LQ, Wang Q - Onco Targets Ther (2016)

Bottom Line: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is identified to be overexpressed in several cancers.A subcutaneous chondrosarcoma cells xenograft model was used to confirm the effect of MALAT-1 on tumor growth in vivo.Finally, we found that MALAT-1 promoted the tumor growth in a subcutaneous chondrosarcoma cells xenograft model, which confirmed the promoted effect of MALAT-1 on the tumor growth in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, Hongquan Hospital, Yangzhou, Jiangsu Province, People's Republic of China.

ABSTRACT

Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is identified to be overexpressed in several cancers. However, the role of MALAT-1 in chondrosarcoma is poorly understood.

Methods: The expression of MALAT-1 and Notch-1 signaling pathway was detected in chondrosarcoma tissues and chondrosarcoma cells by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to examine the cell viability of chondrosarcoma cells transfected with si-MALAT-1 or pcDNA-MALAT-1. Then the expression of Notch-1 signaling pathway was detected when MALAT-1 was upregulated or downregulated in chondrosarcoma cells. A subcutaneous chondrosarcoma cells xenograft model was used to confirm the effect of MALAT-1 on tumor growth in vivo.

Results: We found the increased expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma tissue and cells. MALAT-1 promoted the proliferation of chondrosarcoma cells. In addition, MALAT-1 activated the Notch-1 signaling pathway at posttranscriptional level in chondrosarcoma cells. Meanwhile, overexpression of Notch-1 reversed the effect of si-MALAT-1 on the proliferation of chondrosarcoma cells. Finally, we found that MALAT-1 promoted the tumor growth in a subcutaneous chondrosarcoma cells xenograft model, which confirmed the promoted effect of MALAT-1 on the tumor growth in vivo.

Conclusion: Taken together, our study demonstrated that MALAT-1 promoted the proliferation of chondrosarcoma cell via activating Notch-1 signaling pathway.

No MeSH data available.


Related in: MedlinePlus

The effect of MALAT-1 on the proliferation of chondrosarcoma cells.Notes: (A) The mRNA level of MALAT-1 and cell viability in JJ012 cells with MALAT-1 knockdown. (B) The mRNA level of MALAT-1 and cell viability in CH2879 cells with MALAT-1 overexpression. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.
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f3-ott-9-2143: The effect of MALAT-1 on the proliferation of chondrosarcoma cells.Notes: (A) The mRNA level of MALAT-1 and cell viability in JJ012 cells with MALAT-1 knockdown. (B) The mRNA level of MALAT-1 and cell viability in CH2879 cells with MALAT-1 overexpression. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.

Mentions: Next, JJ012 cells were transfected with si-MALAT-1 to obtain MALAT-1 knockdown, and the cell viability of JJ012 cells were detected. As shown in Figure 3A, the mRNA level of MALAT-1 was significantly decreased by si-MALAT-1, which also greatly suppressed the cell viability of JJ012 cells. Then CH2879 cells were transfected with pcDNA-MALAT-1 to overexpress MALAT-1. It has been shown that the cell viability of CH2879 cells transfected with pcDNA-MALAT-1 was greatly enhanced compared with that of CH2879 cells transfected with pcDNA (Figure 3B). These data indicated that MALAT-1 promoted the proliferation of chondrosarcoma cells.


Metastasis-associated lung adenocarcinoma transcript 1 promotes the proliferation of chondrosarcoma cell via activating Notch-1 signaling pathway.

Xu F, Zhang ZQ, Fang YC, Li XL, Sun Y, Xiong CZ, Yan LQ, Wang Q - Onco Targets Ther (2016)

The effect of MALAT-1 on the proliferation of chondrosarcoma cells.Notes: (A) The mRNA level of MALAT-1 and cell viability in JJ012 cells with MALAT-1 knockdown. (B) The mRNA level of MALAT-1 and cell viability in CH2879 cells with MALAT-1 overexpression. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.
© Copyright Policy
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4835120&req=5

f3-ott-9-2143: The effect of MALAT-1 on the proliferation of chondrosarcoma cells.Notes: (A) The mRNA level of MALAT-1 and cell viability in JJ012 cells with MALAT-1 knockdown. (B) The mRNA level of MALAT-1 and cell viability in CH2879 cells with MALAT-1 overexpression. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.
Mentions: Next, JJ012 cells were transfected with si-MALAT-1 to obtain MALAT-1 knockdown, and the cell viability of JJ012 cells were detected. As shown in Figure 3A, the mRNA level of MALAT-1 was significantly decreased by si-MALAT-1, which also greatly suppressed the cell viability of JJ012 cells. Then CH2879 cells were transfected with pcDNA-MALAT-1 to overexpress MALAT-1. It has been shown that the cell viability of CH2879 cells transfected with pcDNA-MALAT-1 was greatly enhanced compared with that of CH2879 cells transfected with pcDNA (Figure 3B). These data indicated that MALAT-1 promoted the proliferation of chondrosarcoma cells.

Bottom Line: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is identified to be overexpressed in several cancers.A subcutaneous chondrosarcoma cells xenograft model was used to confirm the effect of MALAT-1 on tumor growth in vivo.Finally, we found that MALAT-1 promoted the tumor growth in a subcutaneous chondrosarcoma cells xenograft model, which confirmed the promoted effect of MALAT-1 on the tumor growth in vivo.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedics, Hongquan Hospital, Yangzhou, Jiangsu Province, People's Republic of China.

ABSTRACT

Background: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is identified to be overexpressed in several cancers. However, the role of MALAT-1 in chondrosarcoma is poorly understood.

Methods: The expression of MALAT-1 and Notch-1 signaling pathway was detected in chondrosarcoma tissues and chondrosarcoma cells by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to examine the cell viability of chondrosarcoma cells transfected with si-MALAT-1 or pcDNA-MALAT-1. Then the expression of Notch-1 signaling pathway was detected when MALAT-1 was upregulated or downregulated in chondrosarcoma cells. A subcutaneous chondrosarcoma cells xenograft model was used to confirm the effect of MALAT-1 on tumor growth in vivo.

Results: We found the increased expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma tissue and cells. MALAT-1 promoted the proliferation of chondrosarcoma cells. In addition, MALAT-1 activated the Notch-1 signaling pathway at posttranscriptional level in chondrosarcoma cells. Meanwhile, overexpression of Notch-1 reversed the effect of si-MALAT-1 on the proliferation of chondrosarcoma cells. Finally, we found that MALAT-1 promoted the tumor growth in a subcutaneous chondrosarcoma cells xenograft model, which confirmed the promoted effect of MALAT-1 on the tumor growth in vivo.

Conclusion: Taken together, our study demonstrated that MALAT-1 promoted the proliferation of chondrosarcoma cell via activating Notch-1 signaling pathway.

No MeSH data available.


Related in: MedlinePlus