BackgroundThere remains a great need for effective therapies for cervical cancers, the majority of which are aggressive leaving patients with poor prognosis.Methods and resultsHere, we identify a novel candidate therapeutic target, trefoil factor 3 (TFF3) which overexpressed in cervical cancer cells and was associated with reduced postoperative survival. Functional studies demonstrated that TFF3 overexpression promoted the proliferation and invasion of cervical cancer cells, and inhibited the apoptosis by inducing the mRNA changes in SiHa and Hela cell lines. Conversely, TFF3 silencing disrupted the proliferation and invasion of cervical cancer cells, and induced the apoptosis via Click-iT EdU test, flow cytometry analysis and two-dimensional Matrigel Transwell analysis. Western blot analysis showed that overexpression of TFF3 repressed E-cadherin (CDH1) expression to promote the invasion of cervical cancer cells. Furthermore, down-regulated CDH1 via overexpression of TFF3 was significantly up-regulated by virtue of inhibitor of p-STAT3.ConclusionsThese results suggested that TFF3 stimulated the invasion of cervical cancer cells probably by activating the STAT3/CDH1 signaling pathway. Furthermore, overexpression of TFF3 decreased the sensitivity of cervical cancer cells to etoposide by increasing P-glycoprotein (P-gp) functional activity. Overall, our work provides a preclinical proof that TFF3 not only contributes to the malignant progression of cervical cancers and but also is a potential therapeutic target.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-016-0379-1) contains supplementary material, which is available to authorized users.

1. Congenital long QT syndrome (LQTS) is a genetically heterogeneous disease. The aim of the present study was to identify the gene mutation in a Chinese family with LQTS and investigate the functional changes associated with the mutation. 2. Polymerase chain reaction and DNA sequencing were used to screen for the KCNH2 mutation in the proband. A mutant F463L HERG channel was expressed in HEK293 cells using a lipofectamine method. The IKr current was recorded using the whole-cell voltage clamp technique. Expression of HERG protein was detected by western blotting and the subcellular location of HERG channels in cell was analysed by confocal microscopy. 3. The novel heterozygous missense mutation F463L in KCNH2 was detected. We found that the F463L mutation did not lead to any expression of detectable I(Kr) current, which was consistent with western blotting analysis indicating that the F463L mutation only expressed a band at 135 kDa. When coexpressed with wild-type HERG, F463L HERG exhibited strong dominant-negative current suppression, resulting in a decrease in I(Kr) current density, and induced a positive shift in the voltage dependence of activation, as well as interference with trafficking of wild-type channel protein. The processing of the F463L channels was partly corrected in cells incubated in E4031. In addition, confocal microscopy demonstrated that F463L subunits could be inserted into the cell membrane when forming heteromultimeric channels with wild-type channel subunits. 4. The results of the present study suggest that the F463L mutation leads to loss of function in HERG through a dominant-negative effect caused by impaired trafficking of the channel.

The upregulation of homeobox-B7 (HOXB7) in cancers has been reported. However, its role in oral cancer progression remains to be investigated. In current study, our data revealed that reconstitution of HOXB7 expression by transient transfection resulted in increased cell growth, migration and invasion in vitro. In addition, apoptosis and clonogenic assay data showed that overexpression of HOXB7 decreased the sensitivity of oral cancer cells to vincristine-induced apoptosis of HSC-4 and KB/VCR cells. Furthermore, overexpression of HOXB7 promoted oral cancer cells' migration and invasion through activation of TGFβ2/SMAD3 signaling pathway. Moreover, forced expression of HOXB7 increased Bcl-2 to Bax ratio, which would promote cell survival and induce drug and radiotherapy resistance. Altogether, our findings support the role of HOXB7 in the progression of oral cancer. Therefore, HOXB7 potentially can be a therapeutic target for oral cancer.

Concrete waste was processed into recycled coarse aggregate (RCA), subsequently used to prepare high-strength (>50 MPa) recycled concrete. The resulting material was tested for mechanical performance (ULS). The recycled concrete was prepared to the required design strength by adjusting the water/cement ratio. Concrete containing 0, 20, 50, 80 and 100% recycled aggregate was prepared and studied for workability, deformability and durability. The ultimate aim of the study was to prepare high-strength recycled concrete apt for use in cold climates as a theoretical and experimental basis for the deployment of recycled high-strength concrete in civil engineering and building construction. RESUMEN: Preparación y propiedades del hormigón reciclado de alta resistencia en zonas frías.En este estudio se preparó un hormigón de altas resistencias (>50 MPa) utilizando residuos de hormigón como árido grueso reciclado (RCA). El material resultante se ensayó para determinar sus prestaciones mecánicas (ULS). Para adaptarse a los requerimientos resistentes, se ajustó la relación agua/cemento del hormigón reciclado. Se estudió la trabajabilidad, deformabilidad y durabilidad del hormigón con contenidos del 0, 20, 50, 80 y 100% de árido reciclado. El objetivo final del estudio fue preparar hormigón reciclado de altas resistencias apto para su uso en climas fríos como base teórica y experimental para el desarrollo de este tipo de materiales en obra civil y edificación