Cancer researchers at the
University of Cincinnati (UC) College of Medicine
have found an obesity-associated protein’s role in leukaemia development and
drug response which could lead to more effective therapies for the illness.
The study, published in the online edition of Cancer Cell provided evidence that FTO -- the protein associated with fat mass and obesity -- plays a critical cancer-promoting role by regulating expression of a set of genes through a mechanism involving ribonucleic acid (RNA) modification and thereby increasing the reproduction of leukaemia cells and prohibiting drug response.
Researchers in the study analyzed a
microarray dataset of 100 human acute myeloid leukaemia (AML) samples from
patients and nine normal control samples as well as other large-scale
microarray datasets of AML samples. They found that FTO was highly expressed in
various subtypes of leukaemia samples such as those that contained chromosome
crossover (genetic exchange between chromosomes) or mutations in certain genes.
The high level of FTO expression contributed to cancer cells multiplying and
surviving and also promoted the development of leukemia in animal models and
the non-response of cancer cells to therapeutic agents.
Additionally, researchers found that
genes like ASB2 and RARA, which were reported to inhibit leukaemia cell growth
and/or mediate the response of leukaemia cells to therapeutic agents, were
suppressed in the AML samples with higher FTO expression. The suppression of
these genes was attributed to FTO-controlled decreased stability of their mRNA
and was connected to FTO's m6A demethylase activity.
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