ORCID Profile
0000-0002-1507-5406
Current Organisation
ENN group
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Publisher: Computers, Materials and Continua (Tech Science Press)
Date: 09-2020
DOI: 10.3727/096504020X15861709922491
Abstract: The deubiquitinase cylindromatosis (CYLD) functions as a tumor suppressor inhibiting cell proliferation in many cancer types including melanoma. Here we present evidence that a proportion of melanoma cells are nonetheless addicted to CYLD for survival. The expression levels of CYLD varied widely in melanoma cell lines and melanomas in vivo, with a subset of melanoma cell lines and melanomas displaying even higher levels of CYLD than melanocyte lines and nevi, respectively. Strikingly, although short hairpin RNA (shRNA) knockdown of CYLD promoted, as anticipated, cell proliferation in some melanoma cell lines, it reduced cell viability in a fraction of melanoma cell lines with relatively high levels of CYLD expression and did not impinge on survival and proliferation in a third type of melanoma cell lines. The decrease in cell viability caused by CYLD knockdown was due to induction of apoptosis, as it was associated with activation of the caspase cascade and was abolished by treatment with a general caspase inhibitor. Mechanistic investigations demonstrated that induction of apoptosis by CYLD knockdown was caused by upregulation of receptor-interacting protein kinase 1 (RIPK1) that was associated with elevated K63-linked polyubiquitination of the protein, indicating that CYLD is critical for controlling RIPK1 expression in these cells. Of note, microRNA (miR) profiling showed that miR-99b-3p that was predicted to target the 3-untranslated region (3-UTR) of the CYLD mRNA was reduced in melanoma cell lines with high levels of CYLD compared with melanocyte lines. Further functional studies confirmed that the reduction in miR-99b-3p expression was responsible for the increased expression of CYLD in a highly cell line-specific manner. Taken together, these results reveal an unexpected role of CYLD in promoting survival of a subset of melanoma cells and uncover the heterogeneity of CYLD expression and its biological significance in melanoma.
Publisher: MDPI AG
Date: 11-05-2021
DOI: 10.3390/NANO11051258
Abstract: Quantum scars refer to an enhanced localization of the probability density of states in the spectral region with a high energy level density. Scars are discussed for a number of confined pure and impurity-doped electronic systems. Here, we studied the role of spin on quantum scarring for a generic system, namely a semiconductor-heterostructure-based two-dimensional electron gas subjected to a confining potential, an external magnetic field, and a Rashba-type spin-orbit coupling. Calculating the high energy spectrum for each spin channel and corresponding states, as well as employing statistical methods known for the spinless case, we showed that spin-dependent scarring occurs in a spin-coupled electronic system. Scars can be spin mixed or spin polarized and may be detected via transport measurements or spin-polarized scanning tunneling spectroscopy.
No related grants have been discovered for Zehua SONG.