alexa Elevation of miR-27b by HPV16 E7 inhibits PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells.
Genetics & Molecular Biology

Genetics & Molecular Biology

Journal of Molecular and Genetic Medicine

Author(s): Zhang S, Liu F, Mao X, Huang J, Yang J,

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Abstract MicroRNAs (miRNAs) have been reported to be involved in multiple biological pathways that can influence tumor progression and metastasis. High-risk human papillomavirus (HR-HPVs) is aetiologically correlated to cervical cancer. Recently, miRNAs were reported to be regulated by virus and play pivotal roles in HPV-related tumor progression. However, the underlying mechanism remains poorly understood. In the present study, we report that HPV16 E7 upregulated miR-27b to promote proliferation and invasion in cervical cancer. The results showed that PPARγ, as a target of miR-27b, played a significant role in suppressing cervical cancer progression by downregulating the sodium-hydrogen exchanger isoform 1 (NHE1). It was also shown that the inhibition of miR-27b diminished the ability of HPV16 E7 to suppress PPARγ or activate NHE1 expression. In addition, we observed high expression of miR-27b and NHE1, but low expression of PPARγ in HPV16-positive cervical cancer tissues. In summary, the present study revealed that miR-27b is upregulated by HPV16 E7 to inhibit PPARγ expression and promotes proliferation and invasion in cervical carcinoma cells. This article was published in Int J Oncol and referenced in Journal of Molecular and Genetic Medicine

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