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

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.