Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma.

@article{Riquelme2014FrequentCA,
  title={Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma.},
  author={Erick Riquelme and Milind B. Suraokar and Jaime A Rodriguez and B. Salamanca Mi{\~n}o and Heather Y Lin and David Rice and Anne S. Tsao and Ignacio Wistuba},
  journal={Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer},
  year={2014},
  volume={9 7},
  pages={998-1007}
}
INTRODUCTION Malignant pleural mesothelioma (MPM) is a deadly disease with poor prognosis and few treatment options. We characterized and elucidated the roles of C-MYC and PVT1 involved in the pathogenesis of MPM. METHODS We used small interfering RNA (siRNA)-mediated knockdown in MPM cell lines to determine the effect of C-MYC and PVT1 abrogation on MPM cells undergoing apoptosis, proliferation, and cisplatin sensitivity. We also characterized the expression of microRNAs spanning the PVT1… CONTINUE READING

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Mentioned Connections BETA
Proto-Oncogene Proteins c-mycGene product plays role in biological processCell Proliferation
C - MYC and PVT1 knockdown reduced cell proliferation and increased sensitivity to cisplatin .
C - MYC and PVT1 knockdown reduced cell proliferation and increased sensitivity to cisplatin .
PVT1 geneGene encodes gene productPVT1 Protein
Our results suggest that C - MYC and PVT1 CNG promotes a malignant phenotype of MPM , with C - MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis .
Our results suggest that C - MYC and PVT1 CNG promotes a malignant phenotype of MPM , with C - MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis .
Our results suggest that C - MYC and PVT1 CNG promotes a malignant phenotype of MPM , with C - MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis .
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