RNAi mediated MMP-1 silencing inhibits human chondrosarcoma invasion

Yuan, Jun; Dutton, Charyl M.; Scully, Sean P.

doi:10.1016/j.orthres.2005.04.004.1100230633

Cited by 75 publications

(14 citation statements)

References 35 publications

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“…RNAi technique to silence transcription factors operative in MMP/TIMP expression, this approach may also be applicable in targeting specific MMP/TIMP transcripts directly [120,121]. For example, using adenoviral construct and transfection methods, an RNAi sequence targeted against the MMP-9 mRNA was produced in mammalian cells (glioblastoma cell line) [120].…”

Section: Summary and Future Directionsmentioning

confidence: 99%

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

Deschamps

Spinale²

2006

Cardiovascular Research

167

128

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The structural basis for the development of congestive heart failure (CHF) is a maladaptive myocardial remodeling process which occurs secondarily to post-myocardial infarction (MI), hypertensive hypertrophy, or cardiomyopathy. Both cellular and extracellular factors are involved in the remodeling process and it is the combined action of these factors giving rise to changes in myocardial structure which eventually affects function. One component in this remodeling process is a family of extracellular matrix degrading enzymes, the matrix metalloproteinases or MMPs. Many bioactive molecules such as cytokines/chemokines, bioactive peptides, and neurohormones which are operative in CHF likely contribute to the induction of MMPs. For example, a specific cassette of transcription factors is likely induced with extracellular stimuli in the context of CHF which in turn induces MMPs and contributes to the maladaptive remodeling process. This review will briefly discuss the biology of the MMP family, but will more importantly identify how biological factors active in CHF result in the modulation of the MMP family. Understanding how upstream molecules are involved in MMP regulation/dysregulation may provide an avenue to develop important therapeutic interventions.

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Section: Summary and Future Directionsmentioning

confidence: 99%

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

Deschamps

Spinale²

2006

Cardiovascular Research

167

128

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“…In clinical practice, surgical resection remains the primary mode of therapy. Chondrosarcoma is reported as easily metastasizing to other organs: e.g., lung, liver [3,4]. Distant metastasis means poor prognosis and high incidence of fatality associated with this mesenchymal malignancy due to lack of an effective adjuvant therapy, making it important to explore novel remedies [5,6].…”

Section: Introductionmentioning

confidence: 99%

Paeonol Suppresses Chondrosarcoma Metastasis through Up-Regulation of miR-141 by Modulating PKCδ and c-Src Signaling Pathway

Horng

Shieh

Tan

et al. 2014

IJMS

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Chondrosarcoma, a primary malignant bone cancer, has potential for local invasion and distant metastasis, especially to the lungs. Patients diagnosed with it show poor prognosis. Paeonol (2'-hydroxy-4'-methoxyacetophenone), the main active compound of traditional Chinese remedy Paeonia lactiflora Pallas, exhibits anti-inflammatory and anti-tumor activity; whether paeonol regulates metastatic chondrosarcoma is largely unknown. Here, we find paeonol do not increase apoptosis. By contrast, at non-cytotoxic concentrations, paeonol suppresses migration and invasion of chondrosarcoma cells. We also demonstrate paeonol enhancing miR-141 expression and miR-141 inhibitor reversing paeonol-inhibited cell motility; paeonol also reduces protein kinase C (PKC)δ and c-Src kinase activity. Since paeonol inhibits migration and invasion of human chondrosarcoma via up-regulation of miR-141 via PKCδ and c-Src pathways, it thus might be a novel anti-metastasis agent for treatment of metastatic chondrosarcoma.

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“…Clinically, surgical resection remains the primary mode of therapy for chondrosarcoma. In the absence of an effective adjuvant therapy, this mesenchymal malignancy has a poor prognosis and novel and adequate therapies are needed [2].…”

Section: Introductionmentioning

confidence: 99%

Curcumin induces cell apoptosis in human chondrosarcoma through extrinsic death receptor pathway

Lee

Tsao

et al. 2012

International Immunopharmacology

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RNAi mediated MMP-1 silencing inhibits human chondrosarcoma invasion

Cited by 75 publications

References 35 publications

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

Paeonol Suppresses Chondrosarcoma Metastasis through Up-Regulation of miR-141 by Modulating PKCδ and c-Src Signaling Pathway

Curcumin induces cell apoptosis in human chondrosarcoma through extrinsic death receptor pathway

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