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Ayub, R.

Publications and source records attributed to Ayub, R..

2 recordsLinked to original sources

Finding the neural correlates of collaboration using a three-person fMRI hyperscanning paradigm

Humans have an extraordinary ability to interact and cooperate with others, which plays a pivotal role in societies at large. Despite its potential social and evolutionary significance, research on finding the neural correlates of collaboration has been limited partly due to restrictions on simultaneous neuroimaging of more than one participant (a.k.a. hyperscanning). A series of works now exists that used dyadic fMRI hyperscanning to examine the interaction between two participants. However, to our knowledge, no study to date has aimed at revealing the neural correlates of social interactions using a 3-person (or triadic) fMRI hyperscanning paradigm. Here, for the first time, we simultaneously measured the blood-oxygenation-level-dependent (BOLD) signal of triads (m=12 triads; n=36 participants), while they engaged in a joint drawing task based on the social game of Pictionary(R). General linear model (GLM) analysis revealed increased activation in the brain regions previously linked with the theory of mind (ToM) during the collaborative phase compared to the independent phase of the task. Furthermore, using intersubject brain synchronization (IBS) analysis, we revealed increased synchrony of the right temporo-parietal junction (R TPJ) during the collaborative phase. The increased synchrony in the R TPJ was observed to be positively associated with the overall team performance on the task. In sum, our novel paradigm revealed a vital role of the R TPJ among other ToM regions during a triadic collaborative drawing task.

neuroscience↗

RUNX/CBFβ transcription factor complexes promote the phenotypic plasticity of metastatic breast cancer cells

Epithelial to mesenchymal transition (EMT) is a dynamic process that drives cancer cell plasticity and is thought to play a major role in metastasis. Here we show that the plasticity of metastatic breast cancer cells can be promoted by the activity of the RUNX transcription factors. We demonstrate that the RUNX co-regulator CBF{beta} is essential to maintain the mesenchymal phenotype of triple-negative breast cancer cells and that CBF{beta}-depleted cells undergo a mesenchymal to epithelial transition (MET) and re-organise into acini-like structures, reminiscent of those formed by epithelial breast cells. We subsequently show, using an inducible CBF{beta} system, that the MET can be reversed, thus demonstrating the plasticity of RUNX/CBF{beta}-mediated EMT. Moreover, the MET can be reversed by expression of the EMT transcription factor Slug whose expression is dependent on CBF{beta}, RUNX1 and RUNX2. Finally, we demonstrate that loss of CBF{beta} inhibits the ability of metastatic breast cancer cells to invade bone cell cultures and suppresses their ability to form bone metastases in vivo. Together our findings demonstrate that the RUNX/CBF{beta} complexes can determine the plasticity of the metastatic cancer cell phenotypes, suggesting that their regulation in different micro-environments may play a key role in the establishment of metastatic tumours.

cancer biology↗