The Lattice Distortion-Induced Ferromagnetism in the Chemical-Bonded MoSe2/WSe2 at Room Temperature.

Ferromagnetism to non-ferromagnetism transition is detected in a chemically bonded MoSe[Formula: see text]/WSe[Formula: see text] powder with different thermal annealing temperatures. All samples exhibit ferromagnetism and Raman redshift, except for the 1100 °C thermally annealed sample in which the MoSe[Formula: see text] and WSe[Formula: see text] are thermally dissociated and geometrically separated. The element analysis reveals no significant element ratio difference and detectable magnetic elements in all samples. These results support that, in contrast to the widely reported structure defect or transition element dopant, the observed ferromagnetism originates from the structure distortion due to the chemical bonding at the interface between MoSe[Formula: see text] and WSe[Formula: see text].

The Singularity Paramagnetic Peak of Bi0.3Sb1.7Te3 with p-type Surface State.

The magnetization measurement was performed in the Bi0.3Sb1.7Te3 single crystal. The magnetic susceptibility revealed a paramagnetic peak independent of the experimental temperature variation. It is speculated to be originated from the free-aligned spin texture at the Dirac point. The ARPES reveals that the Fermi level lies below the Dirac point. The Fermi wavevector extracted from the de Haas-van Alphen oscillation is consistent with the energy dispersion in the ARPES. Our experimental results support that the observed paramagnetic peak in the susceptibility curve does not originate from the free-aligned spin texture at the Dirac point.

The High Coercivity Field in Chemically Bonded WSe2/MoSe2 Powder.

We studied the magnetic properties of WSe2/MoSe2 powder. The coercivity field reaches 2600 Oe at 5 K, 4233 Oe at 100 K and 1300 Oe at 300 K. These are the highest values reported for two-dimensional transition metal dichalcogenides. This study is different from the widely reported vacancy and zigzag structure-induced ferromagnetism studies. Importantly, a Raman peak red shift was observed, and that supports the chemical bonding at the interface between WSe2 and MoSe2. The large coercivity field originates from the chemical bonding-induced structural distortion at the interface between WSe2 and MoSe2.

Observation of Landau Level-Dependent Aharonov-Bohm-Like Oscillations in a Topological Insulator.

We study the quantum oscillations in the BiSbTe3 topological insulator. In addition to the Shubnikov-de Haas (SdH) oscillation, the Aharonov-Bohm-like (ABL) oscillations are also observed. The ABL oscillation period is constant at each Landau level (LL) which is determined from the SdH oscillation. The shorter ABL oscillation periods are observed at lower LLs. The oscillation period is proportional to the square root of the LL at temperatures. The ratio of the ABL oscillation period to the effective mass is weak LL dependence. The LL-dependent ABL oscillation might originate from the LL-dependent effective mass.

Activation of fibroblasts by nicotine promotes the epithelial-mesenchymal transition and motility of breast cancer cells.

The tumor microenvironment plays an important role in tumor initiation and progression. It is well documented that nicotine participates in cigarette smoking-related malignancies. Previous studies focused on the effects of nicotine on tumor cells; however, the role of the microenvironment in nicotine-mediated tumorigenesis is poorly understood. Herein, we investigated the effect and molecular mechanism of nicotine on fibroblasts and its contribution to breast cancer. We found that nicotine induced the epithelial-mesenchymal transition (EMT) of breast cancer cells and promoted activation of fibroblasts. Interestingly, conditioned medium from nicotine-activated fibroblasts (Nic-CM) had a greater impact on promoting the EMT and migratory capability toward cancer cells than did treatment with nicotine alone. Production of connective tissue growth factor (CTGF) and transforming growth factor (TGF)-ß by nicotine-treated fibroblasts was demonstrated to be crucial for promoting the EMT and cancer cell migration, and blocking of CTGF and TGF-ß in Nic-CM-suppressed tumor motility. Moreover, nicotine induced expressions of CTGF, and TGF-ß in fibroblasts as identified through α7 nicotinic acetylcholine receptor (nAChR)-dependent activation of the AKT/TAZ signaling mechanism. Together, our data showed for the first time that activation of fibroblasts is largely responsible for accelerating smoking-mediated breast cancer progression.

Panobinostat sensitizes KRAS-mutant non-small-cell lung cancer to gefitinib by targeting TAZ.

Mutation of KRAS in non-small-cell lung cancer (NSCLC) shows a poor response to epidermal growth factor receptor (EGFR) inhibitors and chemotherapy. Currently, there are no direct anti-KRAS therapies available. Thus, new strategies have emerged for targeting KRAS downstream signaling. Panobinostat is a clinically available histone deacetylase inhibitor for treating myelomas and also shows potentiality in NSCLC. However, the therapeutic efficacy of panobinostat against gefitinib-resistant NSCLC is unclear. In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild-type NSCLC. Combined panobinostat and gefitinib synergistically reduced tumor growth in vitro and in vivo. Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Clinically, TAZ was positively correlated with EGFR signaling, and coexpression of TAZ/EGFR conferred a poorer prognosis in lung cancer patients. Our findings identify that targeting TAZ-mediated compensatory mechanism is a novel therapeutic approach to overcome gefitinib resistance in KRAS-mutant/EGFR-wild-type NSCLC.