Exosomal transfer of stroma-derived miR21 confers paclitaxel resistance in ovarian cancer cells through targeting APAF1

Chi Lam Au Yeung, Ngai-Na Co, Tetsushi Tsuruga, Tsz-Lun Yeung, Suet-Ying Kwan, Cecilia S. Leung, Yong Li, Edward S. Lu, Kenny Kwan, Kwong-Kwok Wong, Rosemarie Schmandt, Karen H. Lu and Samuel C. Mok ()
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Chi Lam Au Yeung: The University of Texas MD Anderson Cancer Center
Ngai-Na Co: The University of Texas MD Anderson Cancer Center
Tetsushi Tsuruga: The University of Texas MD Anderson Cancer Center
Tsz-Lun Yeung: The University of Texas MD Anderson Cancer Center
Suet-Ying Kwan: The University of Texas MD Anderson Cancer Center
Cecilia S. Leung: The University of Texas MD Anderson Cancer Center
Yong Li: University of Louisville
Edward S. Lu: The University of Texas MD Anderson Cancer Center
Kenny Kwan: The University of Texas MD Anderson Cancer Center
Kwong-Kwok Wong: The University of Texas MD Anderson Cancer Center
Rosemarie Schmandt: The University of Texas MD Anderson Cancer Center
Karen H. Lu: The University of Texas MD Anderson Cancer Center
Samuel C. Mok: The University of Texas MD Anderson Cancer Center

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Advanced ovarian cancer usually spreads to the visceral adipose tissue of the omentum. However, the omental stromal cell-derived molecular determinants that modulate ovarian cancer growth have not been characterized. Here, using next-generation sequencing technology, we identify significantly higher levels of microRNA-21 (miR21) isomiRNAs in exosomes and tissue lysates isolated from cancer-associated adipocytes (CAAs) and fibroblasts (CAFs) than in those from ovarian cancer cells. Functional studies reveal that miR21 is transferred from CAAs or CAFs to the cancer cells, where it suppresses ovarian cancer apoptosis and confers chemoresistance by binding to its direct novel target, APAF1. These data suggest that the malignant phenotype of metastatic ovarian cancer cells can be altered by miR21 delivered by exosomes derived from neighbouring stromal cells in the omental tumour microenvironment, and that inhibiting the transfer of stromal-derived miR21 is an alternative modality in the treatment of metastatic and recurrent ovarian cancer.

Date: 2016
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DOI: 10.1038/ncomms11150

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