Oncoprotein ZNF322A transcriptionally deregulates alpha-adducin, cyclin D1 and p53 to promote tumor growth and metastasis in lung cancer.

This corrects the article DOI: 10.1038/onc.2015.296.

Oncoprotein ZNF322A transcriptionally deregulates alpha-adducin, cyclin D1 and p53 to promote tumor growth and metastasis in lung cancer.

This corrects the article DOI: 10.1038/onc.2015.296.

Oncoprotein ZNF322A transcriptionally deregulates alpha-adducin, cyclin D1 and p53 to promote tumor growth and metastasis in lung cancer.

ZNF322A encoding a classical Cys2His2 zinc finger transcription factor was previously revealed as a potential oncogene in lung cancer patients. However, the oncogenic role of ZNF322A and its underlying mechanism in lung tumorigenesis remain elusive. Here we show ZNF322A protein overexpression in 123 Asian and 74 Caucasian lung cancer patients. Multivariate Cox regression analysis indicated that ZNF322A was an independent risk factor for a poor outcome in lung cancer, corroborating the Kaplan-Meier results that patients with ZNF322A protein overexpression had significantly poorer overall survival than other patients. Overexpression of ZNF322A promoted cell proliferation and soft agar growth by prolonging cell cycle in S phase in multiple lung cell lines, including the immortalized lung cell BEAS-2B. In addition, ZNF322A overexpression enhanced cell migration and invasion, whereas knockdown of ZNF322A reduced cell growth, invasion and metastasis abilities in vitro and in vivo. Quantitative proteomic analysis revealed potential ZNF322A-regulated downstream targets, including alpha-adducin (ADD1), cyclin D1 (CCND1), and p53. Using luciferase promoter activity assay combined with site-directed mutagenesis and sequential chromatin immunoprecipitation-PCR assay, we found that ZNF322A could form a complex with c-Jun and cooperatively activate ADD1 and CCND1 but repress p53 gene transcription by recruiting differential chromatin modifiers, such as histone deacetylase 3, in an AP-1 element dependent manner. Reconstitution experiments indicated that CCND1 and p53 were important to ZNF322A-mediated promotion of cell proliferation, whereas ADD1 was necessary for ZNF322A-mediated cell migration and invasion. Our results provide compelling evidence that ZNF322A overexpression transcriptionally dysregulates genes involved in cell growth and motility therefore contributes to lung tumorigenesis and poor prognosis.

Effect of disorder on the quantum coherence in mesoscopic wires.

We present phase coherence time measurements in quasi-one-dimensional mesoscopic wires made from high mobility two-dimensional electron gas. By implanting gallium ions into a GaAs/AlGaAs heterojunction we are able to vary the diffusion coefficient over 2 orders of magnitude. We show that in the diffusive limit, the decoherence time follows a power law as a function of diffusion coefficient as expected by theory. When the disorder is low enough so that the samples are semiballistic, we observe a new and unexpected regime in which the phase coherence time is independent of disorder. In addition, for all samples the temperature dependence of the phase coherence time follows a power law down to the lowest temperatures without any sign of saturation and this strongly suggests that the frequently observed low temperature saturation is not intrinsic.

Resistance of a single domain wall in (Co/Pt)7 multilayer nanowires.

Single (Co/Pt)_{7} multilayer nanowires prepared by electron beam lithography with perpendicular magnetic anisotropy are locally modified by means of Ga-ion implantation generating 180 degrees domain walls which are pinned at the edges of underlying thin Pt wires. Since we can exclude contributions from the anisotropic and the Lorentz magnetoresistance this allows us to determine the resistance of a single domain wall at room temperature. We find a positive relative resistance increase of DeltaR/R=1.8% inside the domain wall which agrees well with the model of Levy and Zhang [Phys. Rev. Lett. 79, 5110 (1997)10.1103/PhysRevLett.79.5110].