Objective This study compares the population and repair ability of bone marrow hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) in experimental colitis (EC) rat model after allogeneic stem-cell transplantation (SCT). Methods EC was induced by 2, 4, 6-trinitrobenzenesulfonic acid (TNBS). The HSCs, MSCs, HSCs+MSCs, derived from male Sprague-Dawley rats, were cultured and labeled with bromodeoxyuridine and then transplanted into the EC rat. The colon samples were collected for histologic evaluation at days 7, 14, and 21 posttransplantation. Immunohistochemical staining, polymerase chain reaction, and fluorescence in situ hybridization were used to detect donor stem cells population. Results EC induced by TNBS had characteristics similar to those of Crohn's disease. A large number of bromodeoxyuridine-labeled HSCs or MSCs were detected on days 7, 14, and 21 posttransplantation. Sex-determining region of Y chromosomes (sry) was found in all EC regions, but not in control and normal tissues. A clear localization of Y chromosomes in the colons of EC rat was detected by fluorescence in situ hybridization. Immunohistochemical staining revealed that HSCs or MSCs had similar population ability. When HSCs and MSCs were combined, gross morphologic scores significantly improved 21 days post-SCT compared with the control without SCT, but only slightly better than that of HSCs or MSCs alone. Conclusions Allogeneic transplantation of HSCs or MSCs alone could populate in the injured regions of the colons, both showed similar population ability in the colons of the TNBS-induced EC model rats. Combination transplantation of HSCs with MSCs could improve the gross morphologic scores of EC.

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.

Screening of natural products with anti-tumor activity as telomerase inhibitor is a new subject in the field of tumor therapy. Using telomerase PCR ELISA, telomere DNA hybridization and flow cytometry analysis, the effects of verbascoside, a phenylpropanoid glucoside extracted from Pedicularis striata Pall, on telomerase activity, telomere length and cell cycle of human gastric carcinoma cells MKN45 was examined in vitro. After being treated with a 50 % inhibition concentration of verbascoside (17.8 microg/ml), telomerase activity in the cells was significantly inhibited but not in the cellular supernatant, the average telomere length became remarkably short, and the sub-G0 /G1 peak and G2/M arrest were also displayed when compared to the control cells. These results suggest that verbascoside mediated-cell differentiation and apoptosis may be affected by telomere-telomerase-cell cycle dependent modulation. Thus, the antitumor mechanism of verbascoside is demonstrated once more by its inhibiting effect on telomerase activity in tumor cells, and the telomerase assay may provide a valuable screening method for antitumor activity of natural products.