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abnormal formation and growth of the placenta are considered to be potential causes of various pregnancy complications, such as miscarriage, pre-eclampsia and restricted fetal growth. However, there is still much to be learned about regulating the molecular mechanisms of the organ. Researchers at the University of South Florida have discovered how a very large human non-protein-coded gene regulates endotrin-interstational transformation (EMT), a process that helps placental implants early in pregnancy and the progression and spread of cancer.
researchers used CRISPR genome editing techniques to activate tiny RNA clusters (C19MC) of all chromosome 19 to study the gene's function in the early stages of pregnancy. C19MC is one of the largest clusters of tiny RNA genes in the human genome, usually closed and expressed only in placentas, embryonic stem cells and certain cancers.
in a recent study of cell models published in Scientific Reports, researchers say the strong activation of C19MC inhibits EMT. The researchers found that when placental-forming nourishing layer cells were exposed to hypoxia, the expression of C19MC decreased significantly. The loss of C19MC's function releases nourishing cells that differentiate from stem cell-like endocysts to interstity cells, which can migrate and invade like metastasis tumors.Hana Totary-Jain, senior author of the
article, said: "Our study shows that C19MC plays a key role in the regulation of many genes that play an important role in early embryo implantation, placental development and function, and that the regulation of these genes is critical to the normal growth of the fetus. Experts
the study could help better understand and control pre-eclampsia and fetal growth restrictions, which account for 5 to 10 percent of all pregnancy complications and premature births. Moreover, the study of the effects of C19MC expression changes on cell differentiation and nourishment of cell invasion is also significant for cancer and stem cell research.
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