LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2

Additional file 4: Figure S3. Representative images of colony formation of Mino cells. a The number of colonies in MALAT1 knockdown Mino cells were significantly reduced. b Photographs of colonies in colony formation assay. The size of individual colony was significantly reduced in MALAT1 knockdown Mino cells

Charge Asymmetry and Photon Energy Spectrum in the Decay Bs→l+l−γB_s \to l^+ l^- \gamma

We consider the structure-dependent amplitude of the decay $B_s \to l^+ l^- \gamma$ $(l=e,\mu)$ in a model based on the effective Hamiltonian for $b \bar{s} \to l^+ l^-$ containing the Wilson coefficients $C_7,C_9$ and $C_{10}$. The form factors characterising the matrix elements $< \gamma | \bar{s} \gamma_\mu (1 \mp \gamma_5) b | \bar{B}_s>$ and $< \gamma | \bar{s} \sigma_{\mu\nu} (1 \mp \gamma_5) b | \bar{B}_s>$ are taken to have the universal form $f_V \approx f_A \approx f_T \approx f_{B_s} M_{B_s} R_s / (3 E_\gamma)$ suggested by recent work in QCD, where $R_s$ is a parameter related to the light cone wave function of the $B_s$ meson. Simple expressions are obtained for the charge asymmetry $A(x_\gamma)$ and the photon energy spectrum $d \Gamma/ d x_\gamma (x_\gamma = 2 E_\gamma/M_{B_s})$. The decay rates are calculated in terms of the decay rate of $B_s \to \gamma \gamma$. The branching ratios are estimated to be $Br(B_s \to e^+ e^- \gamma) = 2.0 \times 10^{-8}$ and $Br(B_s \to \mu^+ \mu^- \gamma) = 1.2 \times 10^{-8}$, somewhat higher than earlier estimates.Comment: sign of $f_T$ corrected; new table and figure

Direct CP Violation in B-+ -> pi-+ omega, pi-+ rho0, pi0 rho-+, and in B-bar0(B0) -> pi-+ rho+- With an Enhanced Branching Ratio for pi0 rho0

We present a novel dynamics for generating sizable CP-violating asymmetries in the decays of charged $B^\mp\to \pi^\mp \omega, \pi^\mp\rho^0, \pi^0\rho^\mp$, and in $\bar{B^0}(B^0)\to\pi^\mp\rho^\pm$. The dynamics for the necessary final-state interactions involves the mixing of G-parity eigenstates of the system (\bar{D}^*D,D^*\ol{D}) with the $G=\pm 1$ states of $\pi\omega$ and $\pi\rho$, respectively. The dynamical effect is enhanced by the empirically large branching ratio for decays to $(\bar{D}^*D,D^*\bar{D})$. A correlated result is a markedly enhanced branching ratio for $\bar{B^0}(B^0)\to\pi^0\rho^0$, which has now been observed in two experiments

Lentiviral Mediated Transgenesis by In Vivo Manipulation of Spermatogonial Stem Cells

This report describes a technique for the generation of transgenic mice by in vivo manipulation of spermatogonial stem cells with a high rate of success. Spermatogonial stem cells (SSCs) in pre-pubescent animals were infected in vivo with recombinant lentiviruses expressing EGFP-f and mated with normal females. All male pre-founder mice produced transgenic pups with an overall success rate of over 60%. The transgene was heritable and the pre-founder mice could be used in multiple mating experiments. This technology could be used to perform overexpression/knockdown screens in vivo using bar-coded lentiviruses, thus permitting the design of genetic screens in the mouse. Further, this technology could be adapted to other laboratory animals resulting in the generation of model systems that closely approximate human development and disease

Plakophilin3 Loss Leads to an Increase in PRL3 Levels Promoting K8 Dephosphorylation, Which Is Required for Transformation and Metastasis

The desmosome anchors keratin filaments in epithelial cells leading to the formation of a tissue wide IF network. Loss of the desmosomal plaque protein plakophilin3 (PKP3) in HCT116 cells, leads to an increase in neoplastic progression and metastasis, which was accompanied by an increase in K8 levels. The increase in levels was due to an increase in the protein levels of the Phosphatase of Regenerating Liver 3 (PRL3), which results in a decrease in phosphorylation on K8. The increase in PRL3 and K8 protein levels could be reversed by introduction of an shRNA resistant PKP3 cDNA. Inhibition of K8 expression in the PKP3 knockdown clone S10, led to a decrease in cell migration and lamellipodia formation. Further, the K8 PKP3 double knockdown clones showed a decrease in colony formation in soft agar and decreased tumorigenesis and metastasis in nude mice. These results suggest that a stabilisation of K8 filaments leading to an increase in migration and transformation may be one mechanism by which PKP3 loss leads to tumor progression and metastasis

Fascin overexpression promotes neoplastic progression in oral squamous cell carcinoma

<p>Abstract</p> <p>Background</p> <p>Fascin is a globular actin cross-linking protein, which plays a major role in forming parallel actin bundles in cell protrusions and is found to be associated with tumor cell invasion and metastasis in various type of cancers including oral squamous cell carcinoma (OSCC). Previously, we have demonstrated that fascin regulates actin polymerization and thereby promotes cell motility in K8-depleted OSCC cells. In the present study we have investigated the role of fascin in tumor progression of OSCC.</p> <p>Methods</p> <p>To understand the role of fascin in OSCC development and/or progression, fascin was overexpressed along with vector control in OSCC derived cells AW13516. The phenotype was studied using wound healing, Boyden chamber, cell adhesion, Hanging drop, soft agar and tumorigenicity assays. Further, fascin expression was examined in human OSCC samples (N = 131) using immunohistochemistry and level of its expression was correlated with clinico-pathological parameters of the patients.</p> <p>Results</p> <p>Fascin overexpression in OSCC derived cells led to significant increase in cell migration, cell invasion and MMP-2 activity. In addition these cells demonstrated increased levels of phosphorylated AKT, ERK1/2 and JNK1/2. Our in vitro results were consistent with correlative studies of fascin expression with the clinico-pathological parameters of the OSCC patients. Fascin expression in OSCC showed statistically significant correlation with increased tumor stage (<it>P </it>= 0.041), increased lymph node metastasis (<it>P </it>= 0.001), less differentiation (<it>P </it>= 0.005), increased recurrence (<it>P </it>= 0.038) and shorter survival (<it>P </it>= 0.004) of the patients.</p> <p>Conclusion</p> <p>In conclusion, our results indicate that fascin promotes tumor progression and activates AKT and MAPK pathways in OSCC-derived cells. Further, our correlative studies of fascin expression in OSCC with clinico-pathological parameters of the patients indicate that fascin may prove to be useful in prognostication and treatment of OSCC.</p