Yu-Shiba-Rusinov states assisted by asymmetric Coulomb repulsion in a bipartite molecular device.

Interfacing magnetism with superconducting condensates are promising candidates holding Majorana bound states with which fault-tolerant quantum computation could be implemented. Within this field, understanding the detailed dynamics is important both for fundamental reasons and for the development of innovative quantum technologies. Herein, motivated by a molecular magnet TbPcinteracting with a superconducting Pb(111) substrate, which results in spin-orbital Yu-Shiba-Rusinov (YSR) states, as is affirmed by a theoretical simulation with the aid of the numerical renormalization group technique (see Xia20226388), we study the YSR states and quantum phase transitions (QPTs) in a bipartite molecular device adsorbed on ans-wave superconducting substrate.

[Effects of miR-31-5p on HIF-1α/BNIP3 signaling pathway and the expression of osteoblast-related factors of dental pulp stem cells].

Purpose: To investigate the effects of microRNA-31-5p (miR-31-5p) on the signal pathway of hypoxia inducible factor-1α (HIF-1α)/Bcl-2/adenovirus E1B 19-kDa-interacting protein 3(BNIP3) and the expression of osteoblast-related factors of dental pulp stem cells(DPSCs).

Methods: Human dental pulp stem cells (DPSCs) were cultured in vitro and divided into the control group (no transfection), mimic NC group (transfected with negative control-miR-31-5p), miR-31-5p mimic group (transfected with hsa-miR-31-5p mimic), siRNA NC group (transfected with nonsense siRNA) and miR-31-5p siRNA group (transfected with miR-31-5p siRNA).The expressions of miR-31-5p, HIF-1α, BNIP3, alkaline phosphatase(ALP) and Runt-related transcription factor-2(Runx2) mRNA in DPSCs were detected by real-time fluorescence quantitative PCR; the proliferation of DPSCs was detected by MTT; ALP activity of DPSCs was detected by ALP activity test kit; and the protein expressions of HIF-1α, BNIP3 and Runx2 in DPSCs were detected by Western blot.

CXCL12/CXCR4 facilitates perineural invasion via induction of the Twist/S100A4 axis in salivary adenoid cystic carcinoma.

The activation of CXCL12/CXCR4 axis participated in the progression of multiple cancers, but potential effect in terms of perineural invasion (PNI) in SACC remained ambiguous. In this study, we identified that CXCL12 substantially expressed in nerve cells. CXCR4 strikingly expressed in tumour cells, and CXCR4 expression was closely associated with the level of EMT-associated proteins and Schwann cell hallmarks at nerve invasion frontier in SACC.

CD133+ cancer stem-like cells promote migration and invasion of salivary adenoid cystic carcinoma by inducing vasculogenic mimicry formation.

Cancer stem cells (CSCs) have gained much attention due to their roles in the invasion and metastasis of numerous kinds of human cancers. Here, we showed that the positive expression of CD133, the stemness marker, was positively associated with vasculogenic mimicry (VM) formation, local regional recurrence, distant metastasis and poorer prognosis in salivary adenoid cystic carcinoma (ACC) specimens. Compared with CD133- ACC cells, CD133+ cancer stem-like cells had more migration and invasion capabilities, as well as more VM formation.

Transplantation of autologous mesenchymal stem cells for end-stage liver cirrhosis: a meta-analysis based on seven controlled trials.

Background. The bone marrow-derived mesenchymal stem cells (BM-MSCs) have demonstrated great potential as regenerative medicine in different therapeutic applications. This study aims to pool previous controlled clinical trials to make an update assessment of the effectiveness of BM-MSC transplantation on end-stage liver cirrhosis.

WIP1 stimulates migration and invasion of salivary adenoid cystic carcinoma by inducing MMP-9 and VEGF-C.

The wild-type p53 induced phosphatase 1 (WIP1) is an oncogene overexpressed in a variety of human cancers. Here, we demonstrated that WIP1 silencing reduced MMP-9 and VEGF-C expression as well as migration and invasion of salivary adenoid cystic carcinoma (ACC) cells. Overexpression of MMP-9 or VEGF-C restored migration and invasion in WIP1 knockdown cells, indicating that MMP-9 and VEGF-C are downstream targets of WIP1 signaling.

Snail and Slug collaborate on EMT and tumor metastasis through miR-101-mediated EZH2 axis in oral tongue squamous cell carcinoma.

microRNAs(miRNAs) can regulate epithelial-mesenchymal transition (EMT) through transcription factors, however, little is known whether EMT transcription factors can modulate miRNAs and further induce EMT and cancer metastasis. Here we show that overexpression of Snail and Slug leads to a mesenchymal phenotype and morphology and enhances cell invasion along with stem cell properties in squamous cell carcinoma of oral tongue (OTSCC) cells. Repression of miR-101 expression by Snail and Slug is essential for Snail/Slug-induced malignant phenotypes.

C-kit induces epithelial-mesenchymal transition and contributes to salivary adenoid cystic cancer progression.

Epithelial-mesenchymal transition (EMT) is associated with salivary adenoid cystic cancer (ACC) progression and metastasis. Here, we report that ectopic overexpression of c-kit in ACC cell lines is sufficient for acquisition of mesenchymal traits, enhanced cell invasion, along with stem cell properties defined by the presence of a CD133+/CD44+ cell subpopulation. c-kit positively regulated expression of known EMT inducers, also activating TGF-β to contribute to EMT.

Over-expression of integrin-linked kinase correlates with aberrant expression of Snail, E-cadherin and N-cadherin in oral squamous cell carcinoma: implications in tumor progression and metastasis.

Integrin-linked kinase (ILK), an intracellular protein with serine/threonine protein kinase activities, plays a key role in integrin mediated cell-excellular matrix interactions, regulating cell proliferation, apoptosis, differentiation, and migration. ILK has been implicated in the development and progression in several malignancies. However, the role of ILK and ILK-mediated epithelial-mensenchymal transition (EMT) in the progression of oral squamous cell carcinoma (OSCC) has not been well understood.

Single-nucleotide polymorphisms of integrins are associated with the risk and lymph node metastasis of oral squamous cell carcinoma.

Integrins mediate cell-extracellular matrix (ECM) interaction and play a critical role in cell proliferation, migration, survival, and invasion. Polymorphisms of the Integrin gene can alter integrin protein expression, which may further increase the risk of malignancies or cause poor clinical outcomes. The aim of this study was to investigate the potential associations of single-nucleotide polymorphisms (SNPs) of the integrin gene with the susceptibility and clinicopathologic parameters of oral squamous cell carcinoma (OSCC).