Liensinine, an isoquinoline alkaloid extracted from the seed embryo of Nelumbo nucifera Gaertn, has been shown to exhibit various phrenological effects, including anti‑cancer activity. The aim of this study is to investigate the effects and mechanisms of liensinine in human gastric cancer cells. In this study, we found liensinine can significantly inhibit gastric cancer cell proliferation in vitro and in vivo. Liensinine inducedgastric cancer cell apoptosis by increasing cleaved PARP, caspased 3 and caspased 9. Moreover, liensinine induced cycle arrest by downregulatingcyclinD1/cyclin‑dependent kinase4 and phosphorylated protein kinase B. Furthermore, we found liensinine increases ROS levels and inhibits the PI3K/AKT pathway. These data suggested that liensinine might represent a novel and effective agent against gastric cancer.

Gastric carcinoma (GC) is a prevalent malignant cancer worldwide and is highly lethal due to its fast growth. Hence, treatments to suppress GC cell growth may be applied together with surgery and chemotherapy to increase therapeutic outcome. Previous studies have shown the involvement of some microRNAs (miRNAs or miRs) in the carcinogenesis of GC, whereas a role of miR-132 in regulating the growth of GC has not been reported. Here, we report that overexpression of miR-132 in GC cells decreased FoxO1 protein levels, whereas depletion of miR-132 increased FoxO1 protein levels, without altering FoxO1 transcripts. Bioinformatics analyses showed that miR-132 bound to 3'-untranslated region (3'-UTR) of FoxO1 messenger RNA (mRNA) to prevent its translation, which was confirmed by luciferase reporter assay. Moreover, miR-132-mediated suppression of FoxO1 in GC cells resulted in a significant increase in GC cell growth in vitro and in vivo, while increases in FoxO1 by expression of antisense of miR-132 significantly decreased GC cell growth in vitro and in vivo. Finally, miR-132 levels were found significantly increased in GC specimens, compared to those in paired non-tumor gastric tissue. Together, our data suggest that miR-132 upregulation in GC cells may promote cell growth through suppression of FoxO1 translation.

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BackgroundKeloid is one kind of benign skin disease caused by hyperplasia of fibroblasts and collagen fibrils. It is refractory due to the lack of an effective treatment at present, which puts pressure on seeking a new therapeutic regimen. Mesenchymal stem cells (MSCs) from fetal skin are considered to play a crucial role in scarless healing. Nevertheless, the efficacy of them in keloid disorders remains poorly understood.MethodsKeloid fibroblasts (KFs), human adult dermal fibroblasts (ADFs), and human fetal dermal mesenchymal stem cells (FDMSCs) were isolated to single cells and cultured in Dulbecco’s modified Eagle’s medium (DMEM). ADFs and FDMSCs were used to generate ADF-conditioned medium (A-CM) and FDMSC-conditioned medium (F-CM). The effects of A-CM and F-CM on KFs were tested using MTT assay, BrdU assay, TUNEL assay, quantitative polymerase chain reaction, Western blot, and annexin V-FITC/PI binding assay,.ResultsFDMSCs inhibited the bioactivity of KFs, downregulated the expression of the antiapoptotic protein BCL-2, and upregulated the expression of the proapoptotic protein BAX of KFs by secreting some soluble substances, thus accelerating the apoptosis of KFs.ConclusionF-CM induces apoptosis of KFs, providing a novel treatment strategy for keloid disorders.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-017-0624-0) contains supplementary material, which is available to authorized users.

The regenerative repair of deep-degree (second degree) burned skin remains a notable challenge in the treatment of burn injury, despite improvements being made with regards to treatment modality and the emergence of novel therapies. Fetal skin constitutes an attractive target for investigating scarless healing of burned skin. To investigate the inflammatory response during scarless healing of burned fetal skin, the present study developed a nude mouse model, which was implanted with normal human fetal skin and burned fetal skin. Subsequently, human peripheral blood mononuclear cells (PBMCs) were used to treat the nude mouse model carrying the burned fetal skin. The expression levels of matrix metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinases (TIMP)-1 were investigated during this process. In the present study, fetal skin was subcutaneously implanted into the nude mice to establish the murine model. Hematoxylin and eosin staining was used to detect alterations in the skin during the development of fetal skin and during the healing process of deep-degree burned fetal skin. The expression levels of MMP-9 and TIMP-1 were determined using immunochemical staining, and their staining intensity was evaluated by mean optical density. The results demonstrated that fetal skin subcutaneously implanted into the dorsal skin flap of nude mice developed similarly to the normal growth process in the womb. In addition, the scarless healing process was clearly observed in the mice carrying the burned fetal skin. A total of 2 weeks was required to complete scarless healing. Following treatment with PBMCs, the burned fetal skin generated inflammatory factors and enhanced the inflammatory response, which consequently resulted in a reduction in the speed of healing and in the formation of scars. Therefore, exogenous PBMCs may alter the lowered immune response environment, which is required for scarless healing, resulting in scar formation. In conclusion, the present study indicated that the involvement of inflammatory cells is important during the healing process of deep-degree burned skin, and MMP-9 and TIMP-1 may serve important roles in the process of scar formation.