Deletion of mdig enhances H3K36me3 and metastatic potential of the triple negative breast cancer cells
Chitra Thakur, Yiran Qiu, Qian Zhang, Nicholas J. Carruthers, Miaomiao Yu, Zhuoyue Bi, Yao Fu, Priya Wadgaonkar, Bandar Almutairy, Akimasa Seno, Paul M. Stemmer, Fei Chen
Abstract
. Knockout of mdig resulted in an enhancement of H3K36me3 in the genome and upregulation of some X chromosome-linked genes for cell motility, invasion, and metastasis. Silencing MAGED2, one of the most upregulated and H3K36me3-enriched genes resulted from mdig depletion, can partially reverse the invasive migration of the mdig knockout cells. The anti-metastatic and inhibitory role of mdig on H3K36me3 was cross-validated in another cell line, A549 lung cancer cells. Together, our data suggest that mdig is antagonist against H3K36me3 that enforces expression of genes, such as MAGED2, for cell invasion and metastasis.