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MicroRNA-138 functions as a tumor suppressor in osteosarcoma by targeting differentiated embryonic chondrocyte gene 2.

Jiang B, Mu W, Wang J, Lu J, Jiang S, Li L, Xu H, Tian H - J. Exp. Clin. Cancer Res. (2016)

Bottom Line: MicroRNA-138 (miR-138) has been proven to be a tumor suppressor gene in various types of tumors.Moreover, miR-138 expression was significantly lower in metastatic osteosarcoma tissues than that in non-metastatic tissues.DEC2 was verified as a direct target of miR-138, and DEC2 could reverse the inhibitory effect of miR-138 on osteosarcoma progression.

View Article: PubMed Central - PubMed

Affiliation: Department of Traumatic Orthopaedics, The People 's Hospital of Dongying City of Shandong Province, No 317 Nanyi Road, Dongying, 257091, Shandong, China. baoen_jiang@163.com.

ABSTRACT

Background: MicroRNA-138 (miR-138) has been proven to be a tumor suppressor gene in various types of tumors. However, the expression and the role of miR-138 in human osteosarcoma are still poorly understood. We investigated the function and the underlying mechanism of miR-138 in osteosarcoma.

Methods: The expression of miR-138 in human osteosarcoma tissues and cell lines was detected by real-time PCR analysis. The gain-of-function and loss-of-function experiments were performed on osteosarcoma cell lines to investigate the effects of miR-138 on osteosarcoma progression, and to determine whether differentiated embryonic chondrocyte gene 2 (DEC2) mediates these effects. Cell proliferation, apoptosis and invasion were assessed by MTT, flow cytometry and transwell-matrigel assays. Dual-luciferase reporter assay was used to identify whether DEC2 is a direct target of miR-138.

Results: MiR-138 was significantly downregulated in human osteosarcoma tissues and cell lines. Moreover, miR-138 expression was significantly lower in metastatic osteosarcoma tissues than that in non-metastatic tissues. The in vitro gain-of-function and loss-of-function experiments demonstrated that miR-138 inhibited cell proliferation and invasion, and promoted cell apoptosis of human osteosarcoma cells. DEC2 was verified as a direct target of miR-138, and DEC2 could reverse the inhibitory effect of miR-138 on osteosarcoma progression.

Conclusions: These findings suggested that miR-138 acts as a tumor suppressor in osteosarcoma.miR-138 inhibited cell proliferation and invasion, as well as promoted cell apoptosis of human osteosarcoma cells, at least partially, by inhibiting the expression of DEC2. MiR-138/DEC2 may be a novel therapeutic target in osteosarcoma.

No MeSH data available.


Related in: MedlinePlus

Mir-138 mimic inhibited U2OS cell proliferation and invasion, and promoted cell apoptosis. a Fold change of miR-138 expression in U2OS cells following transfection with the miR-138 mimic. b Cell viability c Cell apoptosis rate d Cell invasion of U2OS cells following transfection with the miR-138 mimic. *P < 0.05 and #P < 0.01 compared with the miR-Ctrl
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Fig2: Mir-138 mimic inhibited U2OS cell proliferation and invasion, and promoted cell apoptosis. a Fold change of miR-138 expression in U2OS cells following transfection with the miR-138 mimic. b Cell viability c Cell apoptosis rate d Cell invasion of U2OS cells following transfection with the miR-138 mimic. *P < 0.05 and #P < 0.01 compared with the miR-Ctrl

Mentions: We performed gain-of-function and loss-of-function experiments to explore the role of miR-138 in human osteosarcoma. To overexpress miR-138, miR-138 mimic was transfected into the U2OS cells, which have low endogenous miR-138 expression. In addition, miR-138 inhibitor was transfected into the MG-63 cells, which exhibit high miR-138 expression, to knock down miR-138 expression. The results from real-time quantitative reverse transcription PCR analysis confirmed the ectopic overexpression of miR-138 in U2OS cells and the depletion of miR-138 expression in MG-63 cells (Figs. 2a and 3a, P < 0.01). 48 h after transfection, the cells were subjected to cell proliferation, apoptosis and invasion assays.Fig 2


MicroRNA-138 functions as a tumor suppressor in osteosarcoma by targeting differentiated embryonic chondrocyte gene 2.

Jiang B, Mu W, Wang J, Lu J, Jiang S, Li L, Xu H, Tian H - J. Exp. Clin. Cancer Res. (2016)

Mir-138 mimic inhibited U2OS cell proliferation and invasion, and promoted cell apoptosis. a Fold change of miR-138 expression in U2OS cells following transfection with the miR-138 mimic. b Cell viability c Cell apoptosis rate d Cell invasion of U2OS cells following transfection with the miR-138 mimic. *P < 0.05 and #P < 0.01 compared with the miR-Ctrl
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4837633&req=5

Fig2: Mir-138 mimic inhibited U2OS cell proliferation and invasion, and promoted cell apoptosis. a Fold change of miR-138 expression in U2OS cells following transfection with the miR-138 mimic. b Cell viability c Cell apoptosis rate d Cell invasion of U2OS cells following transfection with the miR-138 mimic. *P < 0.05 and #P < 0.01 compared with the miR-Ctrl
Mentions: We performed gain-of-function and loss-of-function experiments to explore the role of miR-138 in human osteosarcoma. To overexpress miR-138, miR-138 mimic was transfected into the U2OS cells, which have low endogenous miR-138 expression. In addition, miR-138 inhibitor was transfected into the MG-63 cells, which exhibit high miR-138 expression, to knock down miR-138 expression. The results from real-time quantitative reverse transcription PCR analysis confirmed the ectopic overexpression of miR-138 in U2OS cells and the depletion of miR-138 expression in MG-63 cells (Figs. 2a and 3a, P < 0.01). 48 h after transfection, the cells were subjected to cell proliferation, apoptosis and invasion assays.Fig 2

Bottom Line: MicroRNA-138 (miR-138) has been proven to be a tumor suppressor gene in various types of tumors.Moreover, miR-138 expression was significantly lower in metastatic osteosarcoma tissues than that in non-metastatic tissues.DEC2 was verified as a direct target of miR-138, and DEC2 could reverse the inhibitory effect of miR-138 on osteosarcoma progression.

View Article: PubMed Central - PubMed

Affiliation: Department of Traumatic Orthopaedics, The People 's Hospital of Dongying City of Shandong Province, No 317 Nanyi Road, Dongying, 257091, Shandong, China. baoen_jiang@163.com.

ABSTRACT

Background: MicroRNA-138 (miR-138) has been proven to be a tumor suppressor gene in various types of tumors. However, the expression and the role of miR-138 in human osteosarcoma are still poorly understood. We investigated the function and the underlying mechanism of miR-138 in osteosarcoma.

Methods: The expression of miR-138 in human osteosarcoma tissues and cell lines was detected by real-time PCR analysis. The gain-of-function and loss-of-function experiments were performed on osteosarcoma cell lines to investigate the effects of miR-138 on osteosarcoma progression, and to determine whether differentiated embryonic chondrocyte gene 2 (DEC2) mediates these effects. Cell proliferation, apoptosis and invasion were assessed by MTT, flow cytometry and transwell-matrigel assays. Dual-luciferase reporter assay was used to identify whether DEC2 is a direct target of miR-138.

Results: MiR-138 was significantly downregulated in human osteosarcoma tissues and cell lines. Moreover, miR-138 expression was significantly lower in metastatic osteosarcoma tissues than that in non-metastatic tissues. The in vitro gain-of-function and loss-of-function experiments demonstrated that miR-138 inhibited cell proliferation and invasion, and promoted cell apoptosis of human osteosarcoma cells. DEC2 was verified as a direct target of miR-138, and DEC2 could reverse the inhibitory effect of miR-138 on osteosarcoma progression.

Conclusions: These findings suggested that miR-138 acts as a tumor suppressor in osteosarcoma.miR-138 inhibited cell proliferation and invasion, as well as promoted cell apoptosis of human osteosarcoma cells, at least partially, by inhibiting the expression of DEC2. MiR-138/DEC2 may be a novel therapeutic target in osteosarcoma.

No MeSH data available.


Related in: MedlinePlus