Matrix metalloproteinase 9 (MMP-9) in osteosarcoma: Review and meta-analysis

Wang, Jing; Shi, Qiong; Yuan, Taixian; Song, Qilin; Zhang, Yan; Wei, Qiang; Zhou, Lan; Luo, Jinyong; Zuo, Guo‐Wei; Tang, Min; He, Tong‐Chuan; Weng, Yaguang

doi:10.1016/j.cca.2014.03.023

Cited by 50 publications

(32 citation statements)

References 27 publications

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“…Previous studies have demonstrated that an overexpression of MMP-3 in normal breast epithelium results in invasive tumor formation (19). Additionally, in a recent study, MMP-9 was identified as a potential biomarker for OS (20). The downregulation of MMP-3 and -9 confirms that tumorigenesis is inhibited in UbcH10 knockdown OS cells.…”

Section: Discussionmentioning

confidence: 60%

Lentivirus-mediated RNA interference targeting UbcH10 reduces cell growth and invasion of human osteosarcoma cells via inhibition of Ki-67 and matrix metalloproteinases

Wang

et al. 2015

Oncology Letters

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Abstract. Osteosarcoma (OS) is the most commonly diagnosed primary malignancy affecting the bone. UbcH10 is a cancer-related E2-ubiquitin-conjugating enzyme. An overexpression of UbcH10 is significantly associated with tumor grade and cellular proliferation. However, limited evidence exists with regard to the biological function of UbcH10 in OS. The present study created a UbcH10 knockdown OS cell line using lentivirus-mediated RNA interference. The expression of UbcH10 was significantly reduced in UbcH10-targeted small hairpin RNA-expressing lentivirus OS cells. The downregulation of UbcH10 suppressed OS cell proliferation and colony formation ability via decreased Ki-67 expression. UbcH10 knockdown OS cells exhibited impaired invasion and migration abilities. Furthermore, knockdown of UbcH10 led to decreased levels of matrix metalloproteinase-3 and -9 in OS cells. The present study demonstrated the role of UbcH10 in OS cell proliferation, invasion and migration, which suggests that UbcH10 may be a potential candidate for OS therapy.

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Section: Discussionmentioning

confidence: 60%

Lentivirus-mediated RNA interference targeting UbcH10 reduces cell growth and invasion of human osteosarcoma cells via inhibition of Ki-67 and matrix metalloproteinases

Wang

et al. 2015

Oncology Letters

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“…Although MMP‐9 was reported as a potential biomarker for diagnosing OS, more investigations were undoubtedly needed to confirm its diagnostic value . In this study, we revealed that MMP‐9 might promote tumorigenesis, which provided more evidences to support MMP‐9 as the biomarker for OS.…”

Section: Discussionmentioning

confidence: 61%

Matrix metallopeptidase 9 targeted by hsa‐miR‐494 promotes silybin‐inhibited osteosarcoma

Sun

Cheung

Liu

et al. 2017

Molecular Carcinogenesis

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Osteosarcoma (OS) is the most common malignant tumor that develops in bone. Its mortality is very high. Therefore, study of mechanisms of pathogenesis of the OS is urgently required. Previous studies of microarray showed that the expression levels of matrix metallopeptidase 9 (MMP-9) altered significantly in OS. In addition, overexpression of MMP-9 is recognized as an indicator in cancer. However, the exact roles of MMP-9 in OS are not fully investigated. Thus, we firstly studied the roles of MMP-9 in OS and revealed that silence of MMP-9 inhibited OS cell proliferation as determined by MTT assay and colony formation assay. Secondly, we conducted TUNEL assay and confirmed loss of functions of MMP-9 induced OS cell apoptosis. Next, we used lentivector packaging method to overexpress MMP-9 and found that overexpression of MMP-9 promoted OS cell migration. Fourthly, the results of luciferase assay showed that MMP-9 was targeted by hsa-miR-494, which inhibited OS. Fifthly, we revealed that the levels of hsa-miR-494 were upregulated by the drug silybin which inhibited OS. Finally, we revealed that silybin inhibited OS cell viability by altering the protein levels of β-catenin and Runt-related transcription factor 2 (RUNX2) as determined by western blot and immunocytochemistry (ICC).

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“…A previous study reported that JunD activated cell proliferation via upregulation of cyclin D1 proteins (29), and was also demonstrated to activate matrix metalloproteinase (MMP)-7 and MMP-9 transcription (30,31). MMP-7 and MMP-9 have been suggested to be critical for the metastatic and invasive potential in human malignancies, including osteosarcoma (32)(33)(34)(35). Thus, when combined, these results suggest that SPAG9 may induce osteosarcoma cell proliferation and invasion through JNK-JunD signaling.…”

Section: Discussionmentioning

confidence: 99%

SPAG9 is overexpressed in osteosarcoma, and regulates cell proliferation and invasion through regulation of JunD

Xiao

Yan

et al. 2016

Oncology Letters

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Abstract. Sperm-associated antigen 9 (SPAG9) is a recently characterized oncoprotein that is considered to be involved in several forms of malignant tumor. However, its biological function and expression pattern in human osteosarcoma have not yet been elucidated. In the present study, SPAG9 expression was analyzed in 58 cases of human osteosarcoma by immunohistochemistry. The results demonstrated that SPAG9 was overexpressed in 63.8% (37/58) of osteosarcoma tissues, while normal bone tissues exhibited negative SPAG9 expression. SPAG9 small interfering RNA was employed in the U2OS cell line, which has high endogenous expression, and SPAG9 transfection was performed in the MG63 cell line, which has low endogenous expression. MTT and Matrigel invasion assays demonstrated that SPAG-9-knockdown significantly reduced U2OS cell invasion and proliferation, while SPAG9 transfection enhanced MG63 cell proliferation and invasion. Furthermore, it was observed that SPAG9 positively regulated cyclin D1, phosphorylated-c-Jun NH2-terminal kinase (JNK) and JunD expression. Treatment with the JNK inhibitor, SP600125, abolished the upregulatory effect of SPAG9 on JunD. Taken together, the present study identified SPAG9 as a critical oncoprotein involved in osteosarcoma proliferation and invasion, possibly functioning through JNK-JunD signaling.

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Matrix metalloproteinase 9 (MMP-9) in osteosarcoma: Review and meta-analysis

Cited by 50 publications

References 27 publications

Lentivirus-mediated RNA interference targeting UbcH10 reduces cell growth and invasion of human osteosarcoma cells via inhibition of Ki-67 and matrix metalloproteinases

Lentivirus-mediated RNA interference targeting UbcH10 reduces cell growth and invasion of human osteosarcoma cells via inhibition of Ki-67 and matrix metalloproteinases

Matrix metallopeptidase 9 targeted by hsa‐miR‐494 promotes silybin‐inhibited osteosarcoma

SPAG9 is overexpressed in osteosarcoma, and regulates cell proliferation and invasion through regulation of JunD

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