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Cancer cells grow too fast, exceed normal cells, and spread to distant areas, where they cause metastasis.
it is vital to understand what makes cancer cells so efficient and threatening, after all, stopping them has always been a target of cancer research.
early studies have identified cancer genes, the genes that normally control cell growth, but mutations in these genes can trigger cancer cell production and explain their competitive advantage.
polyactive transcription factor MYC has been named 'typical cancer gene' and has abnormal activity in most human cancers.
, targeting MYC is ideal.
, finding c-MYC inhibitors for treatment has been a problem, and MYC itself has long been considered non-drug-targeted.
In this new study, the researchers made a startling discovery: urethra pathogenic E. coli consumes c-MYC protein from infected cells and tissues, which is the result of accelerating the degradation of c-MYC protein and weakening MYC expression.
findings were made after a decrease in MYC expression was observed in children with acute pyelonephritis.
by screening molecules released by urethra pathogenic E. coli, the researchers found that Lon protease is the main effect of MYC degradation and selective for MYC.
then turned the bacterial strategy into cancer treatment, and showed significant results in two different cancer models.
powerful therapeutic effects on tumor growth and improved survival support the therapeutic potential of this molecule.
, Lon protease has been shown to primarily affect myC's overactive cells, suggesting that its toxic side effects are limited.
next step is for us to look at this molecule in more detail and develop research plans for future clinical trials.
: 1.Daniel S.C. Butler et al. A bacterial protease depletes c-MYC and increases survival in mouse models of bladder and colon cancer. Nature Biotechnology, 2021, doi:10.1038/s41587-020-00805-3. 2.Bacterial degradation of the MYC oncogene: A new cancer treatment strategy?