Big discovery! Huang Suyun/He Chuan discovered the potential molecular mechanism of brain metastasis in breast cancer

Brain metastasis is the main cause of cancer death, but little is known about its molecular mechanisms.
addition, little is known about the role of m6A reader YTHDF3 in human diseases.
A joint paper by Huang Suyun of Virginia Commonwealth University and He Chuan of the University of Chicago published online at Canser Cell, entitled "YTHDF3 Induces the Translation of m6A-Enriched Gene Transcripts to Promote Breast Cancer Brain Metastasis", which showed that YTHDF3 overexisting was clinically associated with brain metastasis in breast cancer patients.
YTHDF3 promotes the interaction of cancer cells with endostropheric cells and astrocytes, the exopedation of the blood-brain barrier, angiogenesis and growth.
the mechanism, YTHDF3 enhances the translation of M6A rich transcripts from ST6GALNAC5, GJA1 and EGFR, all of which are associated with brain transfer.
addition, the over-expression of YTHDF3 in brain metastasis tumors is attributed to an increase in the number of copies of genes and the automatic regulation of non-dependent translation of the YTHDF3 cap in the form of binding to the m6A residue in its own 5'UTR.
study reveals the important role of YTHDF3 in controlling the interaction between cancer cells and the micro-environment of the brain to induce brain metastasis.
brain metastasis occurs in more than 20 percent of all cancer patients and occurs about 200,000 times a year in the United States.
, lung cancer and melanoma are the most common types of primary tumors transferred to the brain.
brain metastasis occurs in 15 to 30 percent of breast cancer patients, and the severity of the disease is reflected in its very low survival rate.
incidence of brain metastasis and its impact on survival raise an urgent need to be met, namely, a better understanding of its mechanisms and new therapies.
cancer cells to make genetic and metastasis changes to gain metastasis.
of these changes is the modification of mRNA transcripts.
N6-thyroid glycoside (m6A) is the most abundant form of internal RNA modification.
the regulatory role of m6A-RNA modification in a variety of cellular functions, such as circadian rhythms, thermal shock reactions, stem cell maintenance and differentiation, and neuron function, is beginning to show.
, writing or removing changes in m6A proteins can lead to changes in cellular processes and play a key role in pathological conditions, including cancer.
recent studies have reported the causal effects of m6A-RNA methylation in maintaining the occurrence of tumors in glioblastoma and other cancers.
role of proteins that use m6A RNA methylation and regulate this process in breast cancer brain metastasis has yet to be explored.
the fate and function of
m6A methylated RNA is primarily mediated by readers, including YTH domain family proteins (YTHDF1, YTHDF2, YTHDF3, and YTHDC1), which can directly bind to and read m6A bits on mRNA.
these recognition proteins affect the stability and translation of mRNA, as well as RNA clipping and output.
several studies have reported that YTHDF3 can improve the translation efficiency of its targets and rely on m6A methylation.
, however, little is known about the biological function and relevance of YTHDF3, and little is known about the exact function and role of YTHDF3 in the pathogenesis of cancer.
, the study's increased expression of YTHDF3 was directly related to brain metastasis in breast cancer and a decrease in survival rates in breast cancer patients.
results showed that the knock-down of YTHDF3 led to a significant reduction in brain metastasis in mouse models.
, a set of YTHDF3 target genes critical to brain metastasis in breast cancer was identified.
, the formation of YTHDF3-mediated brain metastasis depends on the m6A methylation state and the improved translation efficiency of its target transcripts.
, the study identified mechanisms for YTHDF3 over-expression in brain metastasis.
specifically, YTHDF3 promotes the interaction of cancer cells with endoblast cells and astrocytes, the exosepation of the blood-brain barrier, angiogenesis and growth.
mechanism, YTHDF3 enhances the translation of M6A rich transcripts from ST6GALNAC5, GJA1 and EGFR, all of which are associated with brain transfer.
addition, the over-expression of YTHDF3 in brain metastasis tumors is attributed to an increase in the number of copies of genes and the automatic regulation of non-dependent translation of the YTHDF3 cap in the form of binding to the m6A residue in its own 5'UTR.
study reveals the important role of YTHDF3 in controlling the interaction between cancer cells and the micro-environment of the brain to induce brain metastasis.
Coconut Source: Inature Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Met Medical" or "Source: MedSci Original" are owned by Metz Medical and may not be reproduced by any media, website or individual without authorization, and shall be reproduced with the words "Source: Mets Medicine".
all reprinted articles on this website are for the purpose of transmitting more information and clearly indicate the source and author, and media or individuals who do not wish to be reproduced may contact us and we will delete them immediately.
at the same time reproduced content does not represent the position of this site.
leave a message here