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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 expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma cells and control.Notes: (A) The mRNA level of MALAT-1 in chondrosarcoma cells and control. (B) The protein level of Notch-1 and its downstream targets Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells and control. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control cell.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.
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f2-ott-9-2143: The expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma cells and control.Notes: (A) The mRNA level of MALAT-1 in chondrosarcoma cells and control. (B) The protein level of Notch-1 and its downstream targets Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells and control. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control cell.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.

Mentions: To verify the dysregulation of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma, we detected the expression of MALAT-1 and Notch-1, Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells (CH2879, L835, JJ012), and TC28a2 as the control cells. It has been shown that the mRNA level of MALAT-1 was higher in chondrosarcoma cells than that in control cells (Figure 2A). Moreover, the mRNA level of MALAT-1 was highest in JJ012 among the three kinds of chondrosarcoma cells. Consistent with the results in chondrosarcoma tissue, the protein levels of Notch-1 as well as Hes-1, Hey-1, and Hey-2 were significantly enhanced in chondrosarcoma cells (Figure 2B). These data indicated that MALAT-1 and Notch-1 signaling pathway might be involved in the pathology of chondrosarcoma.


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 expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma cells and control.Notes: (A) The mRNA level of MALAT-1 in chondrosarcoma cells and control. (B) The protein level of Notch-1 and its downstream targets Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells and control. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control cell.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

f2-ott-9-2143: The expression of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma cells and control.Notes: (A) The mRNA level of MALAT-1 in chondrosarcoma cells and control. (B) The protein level of Notch-1 and its downstream targets Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells and control. Each value represents the mean ± SD of triplicate wells. **P<0.01, vs control cell.Abbreviations: MALAT-1, metastasis-associated lung adenocarcinoma transcript 1; SD, standard deviation.
Mentions: To verify the dysregulation of MALAT-1 and Notch-1 signaling pathway in chondrosarcoma, we detected the expression of MALAT-1 and Notch-1, Hes-1, Hey-1, and Hey-2 in chondrosarcoma cells (CH2879, L835, JJ012), and TC28a2 as the control cells. It has been shown that the mRNA level of MALAT-1 was higher in chondrosarcoma cells than that in control cells (Figure 2A). Moreover, the mRNA level of MALAT-1 was highest in JJ012 among the three kinds of chondrosarcoma cells. Consistent with the results in chondrosarcoma tissue, the protein levels of Notch-1 as well as Hes-1, Hey-1, and Hey-2 were significantly enhanced in chondrosarcoma cells (Figure 2B). These data indicated that MALAT-1 and Notch-1 signaling pathway might be involved in the pathology of chondrosarcoma.

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