During the cell division process known as mitosis the transmission of chromosomes from a parent cell to its daughter cells is a fundamental method by which genes are inherited. During the third phase (known as anaphase) of this four-phase process the daughter chromosomes separate. The pituitary tumor "transforming gene 1 (PTTG1) protein is critical to mitosis because it helps hold the daughter chromosomes together before entering anaphase. Overexpression of PTTG1 is associated with human thyroid cancer, however the events that trigger PTTG1 accumulation are not well understood.
In a study appearing online on October 12, in advance of publication in the November print issue of the Journal of Clinical Investigation, Sheue-yann Cheng and colleagues from the National Cancer Institute show that, normally, PTTG1 is degraded via its physical association with thyroid hormone beta receptor (TRbeta), which binds thyroid hormone (T3). This degradation allows chromosome separation to proceed during anaphase. However, in a mouse model of thyroid cancer a mutant form of TRbeta, which is unable to bind T3, failed to trigger PTTG1 degradation, resulting in elevated PTTG1 protein levels. This caused abnormalities in the mitotic process such that daughter cells received one or more chromosomes above or below the normal chromosome number (a condition known as aneuploidy), which the authors suggest could contribute to the development of thyroid carcinoma.
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Article adapted by Medical News Today from original press release.
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Journal of Clinical Investigation
In a study appearing online on October 12, in advance of publication in the November print issue of the Journal of Clinical Investigation, Sheue-yann Cheng and colleagues from the National Cancer Institute show that, normally, PTTG1 is degraded via its physical association with thyroid hormone beta receptor (TRbeta), which binds thyroid hormone (T3). This degradation allows chromosome separation to proceed during anaphase. However, in a mouse model of thyroid cancer a mutant form of TRbeta, which is unable to bind T3, failed to trigger PTTG1 degradation, resulting in elevated PTTG1 protein levels. This caused abnormalities in the mitotic process such that daughter cells received one or more chromosomes above or below the normal chromosome number (a condition known as aneuploidy), which the authors suggest could contribute to the development of thyroid carcinoma.
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Article adapted by Medical News Today from original press release.
----------------------------
Journal of Clinical Investigation
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