Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis

SNAI1, a zinc finger transcription factor, not only acts as the master regulator of epithelialmesenchymal transition (EMT) but also functions as a driver of cancer progression, including cell invasion, survival, immune regulation, stem cell properties, and metabolic regulation. The regulation of SNAI1 occurs at the transcriptional, translational, and predominant post-translational levels including phosphorylation, acetylation, and ubiquitination. Here, we discuss the regulation and role of SNAI1 in cancer metastasis, with a particular emphasis on epigenetic regulation and posttranslational modifications. Understanding how signaling networks integrate with SNAI1 in cancer progression will shed new light on the mechanism of tumor metastasis and help develop novel therapeutic strategies against cancer metastasis

Long-term Stabilization of Fiber Laser Using Phase-locking Technique with Ultra-low Phase Noise and Phase Drift

We review the conventional phase-locking technique in the long-term stabilization of the mode-locked fiber laser and investigate the phase noise limitation of the conventional technique. To break the limitation, we propose an improved phase-locking technique with an optic-microwave phase detector in achieving the ultra-low phase noise and phase drift. The mechanism and the theoretical model of the novel phase-locking technique are also discussed. The long-term stabilization experiments demonstrate that the improved technique can achieve the long-term stabilization for the MLFL with ultra-low phase noise and phase drift. The excellent locking performance of the improved phase-locking technique implies that this technique can be used to stabilize the mode-locked fiber laser with the highly stable H-master or optical clock without stability loss

Tackle Epithelial-Mesenchymal Transition with Epigenetic Drugs in Cancer

Epithelial-mesenchymal Transition (EMT) is a de-differentiation process in which epithelial cells lose their epithelial properties to acquire mesenchymal features. EMT is essential for embryogenesis and wound healing but is aberrantly activated in pathological conditions like fibrosis and cancer. Tumor-associated EMT contributes to cancer cell initiation, invasion, metastasis, drug resistance and recurrence. This dynamic and reversible event is governed by EMT-transcription factors (EMT-TFs) with epigenetic complexes. In this review, we discuss recent advances regarding the mechanisms that modulate EMT in the context of epigenetic regulation, with emphasis on epigenetic drugs, such as DNA demethylating reagents, inhibitors of histone modifiers and non-coding RNA medication. Therapeutic contributions that improve epigenetic regulation of EMT will translate the clinical manifestation as treating cancer progression more efficiently