Chinese scholar: A miRNA is an anti-cancer fighter

Release date: 2016-04-28

Acute myeloid leukemia (AML) is one of the most common fast-growing blood and bone marrow cancers. Recently, cancer researchers at the University of Cincinnati (UC) have discovered a specific signaling pathway in microRNA (miR-22) that may bring new therapeutic targets for acute myeloid leukemia. The results of these studies were published in the April 26 issue of Nature Communications.

Acute myeloid leukemia is the most common type of acute leukemia, which occurs when the bone marrow begins to make primordial cells (cells that are not yet fully mature). Normally, these primitive cells develop into white blood cells. However, in AML, these cells are not developed and therefore are not resistant to infection.

The head of the study, Dr. Jianjun Chen, an associate professor of cancer biology at the UC School of Medicine, said that some microRNAs appear to be controlled and play a key role in the development of cancer. Dr. Jianjun Chen graduated from Sichuan University in 1994. He graduated from the Shanghai Institute of Biochemistry of the Chinese Academy of Sciences in June 1999. He then worked as a postdoctoral researcher at the University of Chicago in the United States and joined the Department of Biology at the University of Cincinnati in 2014.

He said: "MicroRNAs constitute a small class of non-coding internal RNAs that control the expression of RNAs (mRNAs) by directing or stopping the targeting of a gene. Cellular organisms use mRNA to express genetic information. Studies have shown that miR-22 is associated with breast cancer and other blood diseases, which sometimes turn into AML, but in this study we found that when it is down-regulated - meaning its function is minimized, it may It is an important anti-tumor guardian in AML.

"When we forced the expression of miR-22, we saw that leukemia cells develop, grow and prosper. miR-22 can target multiple oncogenes (CRTC1, FLT3 and MYCBP) and block certain pathways (CREB and MYC) Down-regulation of miR-22 in AML, or reduced production, is caused by a decrease in the amount of DNA being replicated and/or stopped in the TET1/GFI1/EZH2/SIN3A pathway. Moreover, carrying the miR-22 DNA oligo Nanoparticles of nucleotides (short nucleic acid molecules) prevent the development of leukemia."

Dr. Chen conducted the study using bone marrow transplant samples and animal models. He said that in mammals, the ten-eleven translocation protein (TET1/2/3) helps control gene expression during normal development. TET2 mutations can lead to loss of function and tumor slowing, which has been observed in blood and stem cell cancers.

He said: "We recently reported that TET1 plays an important role in cancer promotion in certain AMLs. In these AMLs, it activates the expression of homeobox genes, a similar large gene family in early embryonic development. It can guide the formation of multibody structures. However, whether TET1 can also act as an inhibitor of cell function in cancer and its role in microRNA expression has rarely been studied."

Dr. Chen said that these findings are very important for targeting common cancers and deadly cancers. He said: "Even with chemotherapy, most ALM patients usually do not survive for more than 5 years, so it is so important to develop new effective therapies based on the underlying mechanisms of the disease. This pathogenesis and AML for drugs The response is unclear. Our study revealed a previously unknown signaling pathway (TET1/GFI1/EZH2/SIN3A?miR-22/CREB-MYC) and provided new insights into the genetic mechanisms that trigger AML, highlighting The potential of miR-22-based AML therapy. Of course, more research is needed on this approach and the method of targeting it."

In January of this year, researchers at the University of Melbourne found that they could stop the development of a malignant tumor of leukemia by targeting a protein that can hold the "cancer cell growth" handbrake. The findings were published in the journal Genes & Development. Related reading: The molecule called "Handbrake" called leukemia.

A protein domain that was once thought to be unimportant may be the key to helping patients fight the recurrence of acute myeloid leukemia (AML). In September last year, researchers at Rice University in the United States collaborated with researchers at Baylor College of Medicine and the MD Anderson Cancer Center at the University of Texas to develop a small molecule that could bring a double blow to the protein. In the international chemical authoritative journal "Angewandte Chemie". Related reading: Authoritative journals: the key to preventing the recurrence of leukemia.

In July 2015, a study conducted by the University of California, San Diego School of Medicine revealed a key role for a protein (previously unknown) in the development and progression of acute myeloid leukemia (AML), cutting off tumor cells and meeting their growth nearby Links between cytokines provide a new target for better treatment of leukemia and other cancers, and the results of the study are published in Cell Stem Cell. Related reading: Cell Supplement: The "post-road" to cut off leukemia.

Source: Biopass

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