4.7 Article

Deletion of mdig enhances H3K36me3 and metastatic potential of the triple negative breast cancer cells

期刊

ISCIENCE
卷 25, 期 10, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.isci.2022.105057

关键词

-

资金

  1. National Institutes of Health (NIH) [R01 ES031822, R01 ES028335, R01 ES028263]
  2. Stony Brook University
  3. NIH [P30 ES020957, P30 CA022453, S10 OD030484]

向作者/读者索取更多资源

This report provides evidence of diminished expression of the mineral dust-induced gene (mdig) in human triple negative breast cancer (TNBC). The study demonstrates that mdig promotes the growth of primary tumors but inhibits metastasis of TNBC cells. The findings also suggest a potential role of mdig in regulating genes related to cell motility, invasion, and metastasis.
In this report, we provide evidence showing diminished expression of the mineral dust-induced gene (mdig), a previously identified oncogenic gene, in human triple negative breast cancer (TNBC). Using a mouse model of orthotopic xenograft of the TNBC MDA-MB-231 cells, we demonstrate that mdig promotes the growth of primary tumors but inhibits metastasis of these cells in vivo. 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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据