MiR-30 suppresses lung cancer cell 95D epithelial mesenchymal transition and invasion through targeted regulating Snail.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-30 suppresses lung cancer cell 95D epithelial mesenchymal transition and invasion through targeted regulating Snail, by M.-J. Fan, Y.-H. Zhong, W. Shen, K.-F. Yuan, G.-H. Zhao, Y. Zhang, S.-K. Wang, published in Eur Rev Med Pharmacol Sci 2017; 21 (11): 2642-2649-PMID: 28678320" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/12883.

MiR-30 suppresses lung cancer cell 95D epithelial mesenchymal transition and invasion through targeted regulating Snail.

OBJECTIVE: As an important factor regulating the epithelial mesenchymal transition (EMT) Snail is associated with lung cancer. Bioinformatics analysis showed that microRNA-30a (miR-30a) may target the 3'-UTR of Snail mRNA. It was exhibited that miR-30a down-regulation was related to tumor size, TNM stage, and poor prognosis of non-small cell lung cancer (NSCLC) patients, which suggests that miR-30a might participate in NSCLC attack. This study aims to explore the role of miR-30a and Snail in NSCLC invasion and metastasis. PATIENTS AND METHODS: NSCLC tumor and para-carcinoma tissues were collected from 46 patients to evaluate the miR-30a and Snail expressions. The targeted relationship between miR-30a and Snail was verified by using dual-luciferase reporter assay. 95D cells were cultured in vitro and transfected with miR-30a mimic or small interfere RNA targeting Snail (si-Snail). The expression of miR-30a, Snail, EMT-related factors, malignant growth, invasion, and apoptosis, were compared. RESULTS: Snail was significantly up-regulated, while miR-30a was significantly reduced in NSCLC tissue. MiR-30a suppressed Snail expression by targeting the 3'-URT of Snail mRNA. 95D cells exhibited significantly higher Snail, N-cadherin, and vimentin levels, while lower miR-30a, E-cadherin, and occludin expressions were compared with 95C cells. 95D cells presented stronger malignant growth and invasive ability, whereas lower background apoptosis than 95C. MiR-30a mimic and/or si-Snail transfection significantly enhanced E-cadherin and occludin expression, while significantly declined N-cadherin and vimentin levels, thus weakening malignant growth and invasion and increasing cell apoptosis. CONCLUSIONS: Snail up-regulated, while miR-30a declined in NSCLC tissue. MiR-30a may suppress Snail expression, restrain EMT, and inhibit lung cancer cell invasion.

Safrole-modulated immune response is mediated through enhancing the CD11b surface marker and stimulating the phagocytosis by macrophages in BALB/c mice.

Safrole, a component of piper betle inflorescence, is a documented rodent hepatocarcinogen and inhibits bactericidal activity and the release of superoxide anion (O(2-)) by polymorphonuclear leukocytes (PMNs). In the present study, we investigated the effects of safrole on immune responses, including natural killer (NK) cell cytotoxicity, phagocytic activity and population distribution of leukocytes from normal BALB/c mice. The cells population (cell surface markers) and phagocytosis by macrophages and monocytes from the peripheral blood mononuclear cells (PBMCs) were determined, and NK cell cytotoxicity from splenocytes of mice after oral treatment with safrole was performed using flow cytometric assay. Results indicated that safrole did not affect the weights of body, spleen and liver when compared with the normal mice group. Safrole also promoted the levels of CD11b (monocytes) and Mac-3 (macrophages) that might be the reason for promoting the activity of phagocytosis. However, safrole reduced the cell population such as CD3 (T cells) and CD19 (B cells) of safrole-treated normal mice by oral administration. Furthermore, safrole elevated the uptake of Escherichia coli-labelled fluorescein isothiocyanate (FITC) by macrophages from blood and significantly stimulated the NK cell cytotoxicity in normal mice in vivo. In conclusions, alterations of the cell population (the increase in monocytes and macrophages, respectively) in safrole-treated normal BALB/c mice might indirectly influence the immune responses in vivo.

The polycystic kidney disease 1 gene product modulates Wnt signaling.

Two distinct signaling pathways, involving Wnt signaling and polycystin, have been found to be critical for normal kidney development. Renal tubulogenesis requires the presence of certain Wnt proteins, whereas mutations in polycystin impede the terminal differentiation of renal tubular epithelial cells, causing the development of large cystic kidneys that characterize autosomal dominant polycystic kidney disease. Polycystin is an integral membrane protein, consisting of several extracellular motifs indicative of cell-cell and cell-matrix interactions, coupled through multiple transmembrane domains to a functionally active cytoplasmic domain. We report here that expression of the C-terminal cytoplasmic domain of polycystin stabilizes soluble endogenous beta-catenin and stimulates TCF-dependent gene transcription in human embryonic kidney cells. Microinjection of the polycystin C-terminal cytoplasmic domain induces dorsalization in zebrafish. Our findings suggest that polycystin has the capacity to modulate Wnt signaling during renal development.

Laparoscopic removal of fish bone.

A patient swallowed a fish bone that perforated the stomach wall and embedded in the head of the pancreas. This was confirmed by computed tomographic imaging. We describe a case of successful fish bone removal using a laparoscopic technique, thus avoiding a laparotomy. The patient recovered well and was discharged from the hospital the next day. This is the first description of such a case.

Wnt signaling and transcriptional control of Siamois in Xenopus embryos.

The Wnt-inducible homeobox gene Siamois is expressed in Xenopus embryos before gastrulation and is necessary for formation of the Spemann organizer. Here we show that 5'-flanking sequences of the Siamois coding region can specifically activate a heterologous reporter gene in dorsovegetal cells, thus mimicking Siamois's endogenous expression. A 245-bp DNA fragment is sufficient for activation by both Wnts and endogenous inducers. A dominant negative form of Xenopus T cell-specific factor 3 (XTCF-3) inhibited promoter activity, indicating that T cell-specific factor (TCF)/lymphocyte enhancer binding factor 1 (LEF-1) signaling is necessary for regulation of Siamois. Mutagenesis of two individual TCF sites in the -245 promoter revealed that the proximal, but not distal, site is necessary for dorsovegetal activation. These observations suggest that Siamois is directly regulated by TCFs during dorsoventral axis determination. Further deletion analysis identified a positive regulatory region that is required for dorsal activation, but not for Wnt inducibility, of the promoter. We also present evidence for autoregulation of Siamois transcription. Furthermore, the Siamois promoter was activated by Wnt signaling in 293T tissue culture cells, demonstrating that regulation of the promoter is functionally conserved.