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The CREB1 gene encodes a pleiotropic transcription factor that frequently dysregulated in cancers. CREB1 can regulates tumour cell status of proliferation or migration, however, the molecular basis for this switch involvement in cell plasticity has not been fully understood. Here, we show that knocking out CREB1 triggered a remarkable effect of epithelial-mesenchymal transition (EMT) and led to the occurrence of inhibited proliferation and enhanced motility in cancer cells. Mechanistically, CREB1-knockout cells showed arrest in the G0/G1 phase as a result of impaired CREB1-dependent transcription of CCAT1 and E2F1. Interestingly, the competition between the coactivator CBP/p300 for CREB1 and p65 leads to the activation of the NF-κB pathway in cells with CREB1 disrupted, which induces an EMT phenotype and .

We explore that two ferromagnetic insulator slabs host a strong twist-induced near-field radiative heat transfer in the presence of twisted magnetic fields. Using the formalism of fluctuational electrodynamics, we find the existence of a large twist-induced thermal switch ratio in large damping conditions and nonmonotonic twist manipulation for heat transfer in small damping conditions, associated with the different twist-induced effects of nonreciprocal elliptic surface magnon-polaritons, hyperbolic surface magnon-polaritons, and twist-nonresonant surface magnon-polaritons. Moreover, the near-field radiative heat transfer can be significantly enhanced by the twist-nonresonant surface magnon-polaritons in the ultrasmall damping condition. Such a twist-induced effect is applicable for other kinds of anisotropic slabs with time-reversal symmetry breaking. Our findings provide a way to twisted and magnetic control in nanoscale thermal management and improve it with twistronic concepts.

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