Weak Decays of Doubly Heavy Baryons: the 1/2→1/21/2\to 1/2 case

Very recently, the LHCb collaboration has observed in the final state $\Lambda_c^+ K^-\pi^+\pi^+$ a resonant structure that is identified as the doubly-charmed baryon $\Xi_{cc}^{++}$. Inspired by this observation, we investigate the weak decays of doubly heavy baryons $\Xi_{cc}^{++}$, $\Xi_{cc}^{+}$, $\Omega_{cc}^{+}$, $\Xi_{bc}^{(\prime)+}$, $\Xi_{bc}^{(\prime)0}$, $\Omega_{bc}^{(\prime)0}$, $\Xi_{bb}^{0}$, $\Xi_{bb}^{-}$ and $\Omega_{bb}^{-}$ and focus on the decays into spin $1/2$ baryons in this paper. At the quark level these decay processes are induced by the $c\to d/s$ or $b\to u/c$ transitions, and the two spectator quarks can be viewed as a scalar or axial vector diquark. We first derive the hadronic form factors for these transitions in the light-front approach and then apply them to predict the partial widths for the semi-leptonic and non-leptonic decays of doubly heavy baryons. We find that a number of decay channels are sizable and can be examined in future measurements at experimental facilities like LHC, Belle II and CEPC.Comment: 40 pages, 4 figures, to appear in EPJ

TRIM47 promotes ovarian cancer cell proliferation, migration, and invasion by activating STAT3 signaling

Objectives: Tripartite Motif 47 (TRIM47) protein plays a prominent role in many cancers. This study aimed to investigate the biological roles of TRIM47 in ovarian cancer. Methods: TRIM47 was knocked down and overexpressed in ovarian cancer cell lines SKOV3 and OVCAR3, and the effects on proliferation, clone formation, apoptosis, invasion, and growth of xenograft tumors in nude mice were determined. The expression levels of the selected candidates were tested by western blotting and quantitative real-time PCR. Results: TRIM47 knockdown suppressed proliferation and encourages apoptosis of ovarian cancer cells. Similarly, TRIM47 knockdown suppressed ovarian cancer cell invasion, migration, and epithelial-mesenchymal transition. Ovarian cancer cell xenograft assays demonstrated that TRIM47 knockdown significantly inhibited tumor growth. Mechanistically, TRIM47 knockdown suppressed STAT3 phosphorylation and the expression of several downstream genes, including MCL-1, MMP2, and c-MYC. Silencing of STAT3 partially prevented TRIM47–induced tumor cell proliferation and invasion. Conclusion: The present study's findings demonstrate that by activating STAT3 signaling, TRIM47 functions as an oncogene in ovarian cancer. TRIM47, therefore, appears to be a potential target for ovarian cancer prevention and/or therapy