Constraints on hard spectator scattering and annihilation corrections in Bu,dB_{u,d} →{\to} PVPV decays within QCD factorization

In this paper, we investigate the contributions of hard spectator scattering and annihilation in $B\to PV$ decays within the QCD factorization framework. With available experimental data on $B\to \pi K^{\ast}$, $\rho K$, $\pi \rho$ and $K\phi$ decays, comprehensive $\chi^2$ analyses of the parameters $X_{A,H}^{i,f}({\rho}_{A,H}^{i,f},{\phi}_{A,H}^{i,f})$ are performed, where $X_A^f$ ($X_A^i$) and $X_H$ are used to parameterize the endpoint divergences of the (non)factorizable annihilation and hard spectator scattering amplitudes, respectively. Based on $\chi^2$ analyses, it is observed that (1) The topology-dependent parameterization scheme is feasible for $B\to PV$ decays; (2) At the current accuracy of experimental measurements and theoretical evaluations, $X_H=X_A^i$ is allowed by $B\to PV$ decays, but $X_{H}\neq X_A^f$ at $68$ C. L.; (3) With the simplification $X_H=X_A^i$, parameters $X_A^f$ and $X_A^i$ should be treated individually. The above-described findings are very similar to those obtained from $B\to PP$ decays. Numerically, for $B\to PV$ decays, we obtain $(\rho_{A,H}^i,\phi_{A,H}^i[^{\circ}]) =(2.87^{+0.66}_{-1.95}, -145^{+14}_{-21})$ and $(\rho_A^f,\phi_A^f[^{\circ}]) = (0.91^{+0.12}_{-0.13}, -37^{+10}_{-9})$ at $68$ C. L.. With the best-fit values, most of the theoretical results are in good agreement with the experimental data within errors. However, significant corrections to the color-suppressed tree amplitude $\alpha_2$ related to a large $\rho_H$ result in the wrong sign for $A^{dir}_{CP}(B^- \to \pi^0 K^{{\ast}-})$ compared with the most recent BABAR data, which presents a new obstacle in solving "$\pi\pi$" and "$\pi K$" puzzles through $\alpha_2$. A crosscheck with measurements at Belle (or Belle II) and LHCb, which offer higher precision, is urgently expected to confirm or refute such possible mismatch.Comment: 17 pages, 4 figures; Accepted for publication in PL

Two Iterative algorithms for the matrix sign function based on the adaptive filtering technology

In this paper, two new efficient algorithms for calculating the sign function of the large-scale sparse matrix are proposed by combining filtering algorithm with Newton method and Newton Schultz method respectively. Through the theoretical analysis of the error diffusion in the iterative process, we designed an adaptive filtering threshold, which can ensure that the filtering has little impact on the iterative process and the calculation result. Numerical experiments are consistent with our theoretical analysis, which shows that the computational efficiency of our method is much better than that of Newton method and Newton Schultz method, and the computational error is of the same order of magnitude as that of the two methods.Comment: 18 pages,12 figure

G9a Is Essential for EMT-Mediated Metastasis and Maintenance of Cancer Stem Cell-Like Characters in Head and Neck Squamous Cell Carcinoma

Head and neck squamous cell carcinoma (HNSCC) is a particularly aggressive cancer with poor prognosis, largely due to lymph node metastasis and local recurrence. Emerging evidence suggests that epithelial-to-mesenchymal transition (EMT) is important for cancer metastasis, and correlated with increased cancer stem cells (CSCs) characteristics. However, the mechanisms underlying metastasis to lymph nodes in HNSCC is poorly defined. In this study, we show that E-cadherin repression correlates with cancer metastasis and poor prognosis in HNSCC. We found that G9a, a histone methyltransferase, interacts with Snail and mediates Snail-induced transcriptional repression of E-cadherin and EMT, through methylation of histone H3 lysine-9 (H3K9). Moreover, G9a is required for both lymph node-related metastasis and TGF-β-induced EMT in HNSCC cells since knockdown of G9a reversed EMT, inhibited cell migration and tumorsphere formation, and suppressed the expression of CSC markers. Our study demonstrates that the G9a protein is essential for the induction of EMT and CSC-like properties in HNSCC. Thus, targeting the G9a-Snail axis may represent a novel strategy for treatment of metastatic HNSCC

Autocrine Epiregulin Activates EGFR Pathway for Lung Metastasis Via EMT in Salivary Adenoid Cystic Carcinoma

Salivary adenoid cystic carcinoma (SACC) is characterized by invasive local growth and a high incidence of lung metastasis. Patients with lung metastasis have a poor prognosis. Treatment of metastatic SACC has been unsuccessful, largely due to a lack of specific targets for the metastatic cells. In this study, we showed that epidermal growth factor receptors (EGFR) were constitutively activated in metastatic lung subtypes of SACC cells, and that this activation was induced by autocrine expression of epiregulin (EREG), a ligand of EGFR. Autocrine EREG expression was increased in metastatic SACC-LM cells compared to that in non-metastatic parental SACC cells. Importantly, EREG-neutralizing antibody, but not normal IgG, blocked the autocrine EREG-induced EGFR phosphorylation and the migration of SACC cells, suggesting that EREG-induced EGFR activation is essential for induction of cell migration and invasion by SACC cells. Moreover, EREG-activated EGFR stabilized Snail and Slug, which promoted EMT and metastatic features in SACC cells. Of note, targeting EGFR with inhibitors significantly suppressed both the motility of SACC cells in vitro and lung metastasis in vivo. Finally, elevated EREG expression showed a strong correlation with poor prognosis in head and neck cancer. Thus, targeting the EREG-EGFR-Snail/Slug axis represents a novel strategy for the treatment of metastatic SACC even no genetic EGFR mutation