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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 expression of Notch-1 in chondrosarcoma cells.Notes: (A) The expression of Notch-1 signaling pathway in JJ012 cells treated with si-MALAT-1. (B) The effect of si-MALAT-1 on the degradation of Notch-1 induced by cycloheximide. (C) The expression of Notch-1 signaling pathway in CH2879 cells treated with pcDNA-MALAT-1. (D) RNA pull-down assay was performed to test the binding of MALAT-1 and Notch-1. 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; h, hours.
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f4-ott-9-2143: The effect of MALAT-1 on the expression of Notch-1 in chondrosarcoma cells.Notes: (A) The expression of Notch-1 signaling pathway in JJ012 cells treated with si-MALAT-1. (B) The effect of si-MALAT-1 on the degradation of Notch-1 induced by cycloheximide. (C) The expression of Notch-1 signaling pathway in CH2879 cells treated with pcDNA-MALAT-1. (D) RNA pull-down assay was performed to test the binding of MALAT-1 and Notch-1. 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; h, hours.

Mentions: To investigate the regulated effect of MALAT-1 on the Notch-1 signaling pathway, JJ012 cells were transfected with si-MALAT-1, then the mRNA level of Notch-1 and the protein level of Notch-1 and Hes-1, Hey-1, and Hey-2 were detected. As shown in Figure 4A, si-MALAT-1 exhibited no significant effect on the mRNA level of Notch-1 whereas the protein levels of Notch-1 and Hes-1, Hey-1, and Hey-2 were reduced by si-MALAT-1. Cycloheximide (CHX) is a well-known inhibitor of protein biosynthesis in vivo and in vitro. si-MALAT-1 further accelerated the degradation of Notch-1 induced by CHX (Figure 4B). Moreover, the expression of Notch-1 signaling pathways was examined in CH2879 cells transfected with pcDNA-MALAT-1. Overexpression of MALAT-1 enhanced the protein level of Notch-1 and Hes-1, Hey-1, and Hey-2 (Figure 4C). To further elucidate the relationship between MALAT-1 and Notch-1, RNA pull-down assay was performed and the results indicated that MALAT-1 could bind to Notch-1 (Figure 4D). These results indicated that MALAT-1 could activate the Notch-1 signaling pathway at posttranscriptional level.


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 expression of Notch-1 in chondrosarcoma cells.Notes: (A) The expression of Notch-1 signaling pathway in JJ012 cells treated with si-MALAT-1. (B) The effect of si-MALAT-1 on the degradation of Notch-1 induced by cycloheximide. (C) The expression of Notch-1 signaling pathway in CH2879 cells treated with pcDNA-MALAT-1. (D) RNA pull-down assay was performed to test the binding of MALAT-1 and Notch-1. 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; h, hours.
© Copyright Policy
Related In: Results  -  Collection

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

f4-ott-9-2143: The effect of MALAT-1 on the expression of Notch-1 in chondrosarcoma cells.Notes: (A) The expression of Notch-1 signaling pathway in JJ012 cells treated with si-MALAT-1. (B) The effect of si-MALAT-1 on the degradation of Notch-1 induced by cycloheximide. (C) The expression of Notch-1 signaling pathway in CH2879 cells treated with pcDNA-MALAT-1. (D) RNA pull-down assay was performed to test the binding of MALAT-1 and Notch-1. 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; h, hours.
Mentions: To investigate the regulated effect of MALAT-1 on the Notch-1 signaling pathway, JJ012 cells were transfected with si-MALAT-1, then the mRNA level of Notch-1 and the protein level of Notch-1 and Hes-1, Hey-1, and Hey-2 were detected. As shown in Figure 4A, si-MALAT-1 exhibited no significant effect on the mRNA level of Notch-1 whereas the protein levels of Notch-1 and Hes-1, Hey-1, and Hey-2 were reduced by si-MALAT-1. Cycloheximide (CHX) is a well-known inhibitor of protein biosynthesis in vivo and in vitro. si-MALAT-1 further accelerated the degradation of Notch-1 induced by CHX (Figure 4B). Moreover, the expression of Notch-1 signaling pathways was examined in CH2879 cells transfected with pcDNA-MALAT-1. Overexpression of MALAT-1 enhanced the protein level of Notch-1 and Hes-1, Hey-1, and Hey-2 (Figure 4C). To further elucidate the relationship between MALAT-1 and Notch-1, RNA pull-down assay was performed and the results indicated that MALAT-1 could bind to Notch-1 (Figure 4D). These results indicated that MALAT-1 could activate the Notch-1 signaling pathway at posttranscriptional level.

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