Molecular mechanisms of MCM3AP-AS1 targeted the regulation of miR-708-5p on cell proliferation and apoptosis in gastric cancer cells.

The article "Molecular mechanisms of MCM3AP-AS1 targeted the regulation of miR-708-5p on cell proliferation and apoptosis in gastric cancer cells, by H. Wang, T. Xu, L. Wu, H.-L. Xu, R.-M. Liu, published in Eur Rev Med Pharmacol Sci 2020; 24 (5): 2452-2461-DOI: 10.26355/eurrev_202003_20512-PMID: 32196596" has been withdrawn from the authors due to the discovery of new results. The authors decided to improve them further. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20512.

Molecular mechanisms of MCM3AP-AS1 targeted the regulation of miR-708-5p on cell proliferation and apoptosis in gastric cancer cells.

OBJECTIVE: Gastric cancer (GC) is a common malignancy of the digestive tract. Accumulated studies proved that long non-coding RNA MCM3AP-AS1 (MCM3AP-AS1) modified the mechanism of the progression of GC. However, the molecular mechanism is still greater elusive. Hence, we aimed to explore the molecular mechanism of MCM3AP-AS1 targeting the regulation of microRNA-708-5p on cell proliferation and apoptosis in GC cells. MATERIALS AND METHODS: The expression levels of MCM3AP-AS1 (MCM3AP antisense RNA 1) in gastric mucosal cells GES-1 and gastric cancer cell lines of MGc-803 and SGC-7901 cells were detected by qRT-PCR. Moreover, the protein levels of Cyclin D1, P21, Bax and Bcl-2 in MGc-803 and SGC-7901 cells after transfection were detected by Western blot. MTT assay was performed to detect cell proliferation and flow cytometry was carried out to determine GC cell apoptosis in vitro. In the endpoint, the targeting relationship between MCM3AP-AS1 and microRNA-708-5p was detected by Dual-Luciferase reporter assay. RESULTS: The level of MCM3AP-AS1 was significantly promoted in GC cell lines. Knockdown of MCM3AP-AS1 curbed cell proliferation and enhanced apoptosis in MGc-803 and SGC-7901 cells. Furthermore, the effect of the downregulation of MCM3AP-AS1 on cell proliferation and apoptosis was reversed by knockdown of miR-708-5p, which was targeted by MCM3AP-AS1 in vitro. CONCLUSIONS: MCM3AP-AS1 regulates the proliferation and apoptosis of gastric cancer cells by targeting the expression of microRNA-708-5p. The study may be useful to the therapy target of human GC.

Comparison of effects of devascularization versus shunt on patients with portal hypertension: a meta-analysis.

OBJECTIVE: To systematically evaluate the effectiveness of devascularization and shunt on patients with portal hypertension. METHODS: Relevant studies compared devascularization and shunt for the treatment of portal hypertension were identified searching the PubMed, Embase, Elsevier, CNKI (China National Knowledge Infrastructure) database and Cochrane Trial Register searches until December 2013. Data of interest for devascularization and shunt including postoperative recurrent bleeding, postoperative hepatic encephalopathy,ascites, operative mortality rate, and long term survival rate were subjected to meta-analysis. RESULTS: Eleven studies were included in the study, the results of the meta-analysis showed that all eleven clinical studies demonstrated a significantly higher postoperative recurrent bleeding rate with devascularization group than with shunt group (Odds Ratio =2.14, 95% CI =(1.42, 3.21), P = 0.0003),the rate of hepatic encephalopathy in the devascularization group was significantly lower compared with the shunt group (Odds Ratio =0.56, 95% CI =(0.38, 0.82), P = 0.003); Our meta-analysis of three clinical studies revealed that the reduction of ascites in the devascularization group was significantly less than the shunt groups (Odds Ratio =0.48, 95% CI =(0.26, 0.89), P = 0.02), the operative mortality rate was not significantly different between the devascularization group than for shunt group (Odds Ratio =1.54, 95% CI = (0.91,2.63), P = 0.11). And the long-term survival rate was not significantly different between the devascularization and shunt groups (Odds=1.13, ratio, 95% CI =(0.64, 1.99), P = 0.68). CONCLUSIONS: Devascularization and shunt have different advantages and disadvantages respectively which reflected in postoperative complications and long term survival rate.

Inadequate values from an interferon-gamma release assay for smear-negative tuberculosis in a high-burden setting.

OBJECTIVE: To examine the usefulness of an interferon-gamma release assay (IGRA) for the diagnosis of smear-negative tuberculosis (TB) in China. DESIGN: A total of 624 patients with presumed pulmonary TB were enrolled prospectively and categorised as smear-negative TB, smear-positive TB or no TB. All patients were tested using T-SPOT.TB. RESULTS: Both the smear-negative and smear-positive TB groups had significantly more spot-forming cells (SFCs) than the no TB group (all P < 0.001), while the smear-negative group had fewer SFCs than the smear-positive TB group (P < 0.001). The specificity of T-SPOT.TB was 60.4% (95%CI 53.4-67.1). The sensitivities of T-SPOT.TB in the smear-negative and smear-positive TB groups were respectively 81.4% (95%CI 75.7-86.0) and 93.2% (95%CI 87.6-96.4). The sensitivity in the smear-negative TB group was much lower than that in the smear-positive TB (P < 0.05). CONCLUSIONS: The sensitivity of T-SPOT.TB was lower due the paucibacillary nature of the samples, and the specificity was lower due to the high prevalence of latent tuberculous infection in the smear-negative TB patients. The T-SPOT.TB test should only be used as a supplementary test and not as a single test to rule in or rule out smear-negative TB.

The application of chromosome abnormality chip detection in male infertility / Aplicación de la detección de la anormalidad del cromosoma mediante biochips genéticos en la infertilidad masculina

OBJECTIVE: To discuss the application of microarray technology in the diagnosis of male infertility. METHODS: Sixteen loci, including a sex-determining region on the Y chromosome, were investigated by polymerase chain reaction (PCR) in infertile male patients. Chromosome abnormality chip with 180 000 probes was used to detect small deletion, small amplification and loss of heterozygosity. RESULTS: By PCR, nine of 103 infertile patients were found to have sequence-tagged site microdeletions. Microdeletions were not observed in control samples. The deletions detected by PCR were present in six azoospermic men (6/44, 13.6%) and in three oligoasthenoteratozoospermic (OATS) men (3/59, 5%). The overall frequency of microdeletions in infertile men was 8.7% (9/103). Chromosome abnormality chip detection 500+ detected more amplification or deletion in 51 infertile patients and the overall frequency of microdeletions in infertile men was 49.5% (51/103). CONCLUSION: Chromosome abnormality chip detection system provides a sensitive, economic and high-throughput method for detecting the deletion or amplification of genomic DNA sequences of infertile patients. Not only can it identify Yq deletions, but it can also find other chromosome abnormalities and facilitate the understanding of male infertility.

OBJETIVO: Analizar la aplicación de la tecnología de los microarreglos en el diagnóstico de la infertilidad masculina. MÉTODOS: Dieciséis loci, incluyendo una región determinante del sexo en el cromosoma Y, fueron investigados mediante reacción en cadena de la polimerasa (RCP) en pacientes hombres con problemas de infertilidad. Un biochip de la anormalidad cromosómica, con 180000 sondas, fue utilizado a fin de detectar pequeñas delecciones, pequeñas amplificaciones y pérdidas de heterocigosidad. RESULTADOS: Por medio de la RCP, se halló que nueve de 103 pacientes con infertilidad presentaban microdelecciones de sitios de secuencia marcada. Las microdelecciones no fueron observadas en las muestras de control. Las delecciones detectadas mediante RCP, estuvieron presentes en seis hombres azoospérmicos (6/44, 13.6%) y en tres hombres con oligoastenoteratozoospermia (OAT) (3/59, 5%). La frecuencia general de las microdelecciones en los hombres infértiles fue 8.7% (9/103). La detección con biochip de la anormalidad cromosómica de 500+ detectó más amplificación y delección en 51 pacientes, y la frecuencia general de microdelecciones en los hombres infértiles fue 49.5% (51/103). CONCLUSIÓN: El sistema de detección de la anormalidad del cromosoma mediante biochips genéticos representa un método sensible, económico, y de alto rendimiento, para detectar la delección o amplificación de las secuencias genómicas de ADN de pacientes infértiles. Este método puede no sólo identificar las delecciones Yq, sino también hallar otras anormalidades cromosómicas, facilitando así la comprensión de la infertilidad en los hombres.

Transfer of Ser7 phosphorylated CENP-A from centromere to midbody during mitosis in MCF-7 cells.

Serine 7 of centromere protein A (CENP-A) is a very important mitosis-specific phosphorylation site. In this study, we demonstrate the subcellular distribution of Ser7 phosphorylated CENP-A during mitosis in MCF-7 cells. The Ser7 phosphorylation of CENP-A was observed beginning at prophase at centromeres. Upon progression of mitosis, the fluorescence signals emerged in the central region of the metaphase plate and were maintained until anaphase at centromeres. At late anaphase, the fluorescence signals moved to the midzone gradually and transferred from the centromere to the midbody completely at telophase. They were compacted into the centre of the midbody in a thin cylinder consisting of a sandglass-like "mitotic machine" with microtubules and condensed chromosome. We also found that Ser10 phosphorylated H3 and Thr11 phosphorylated H3 were co-localized at the midbody in two bell-like symmetrical bodies with Ser7 phosphorylated CENP-A during the terminal stage of cytokinesis. Midbody isolation and immunoblotting experiments also indicated that Ser7 phosphorylated CENP-A are components of the midbody. These findings suggest that Ser7 phosphorylated CENP-A acts as a chromosomal passenger protein and may play an important role in cytokinesis.

Neurofibromatosis type-1 with retroperitoneal stromal tumour: one case report.

BACKGROUND: Neurofibromatosis with gastrointestinal stromal tumours have been reported several times, while neurofibromatosis with retroperitoneal stromal tumours are very rare. CASE DESCRIPTION: We report the case of a 44-year-old man with a long history of neurofibromatosis. He complained of severe constipation and left leg pain. The patient's examination showed prominent peripheral cutaneous neurofibromas mainly in the belly and limbs, especially a huge mass in his abdomen, no less than ten café-au-lait spots, four Lisch nodules of the iris. Computed tomography and magnetic resonance imaging revealed a round and lobular mass in the retroperitoneal space. It was a well-circumscribed, hypervascular mass with cystic necrosis. A surgical resection was performed, and pathology and immunohistochemistry findings were consistent with stromal tumour. The c-kit gene and platelet-derived growth factor receptor-α gene mutations are not observed in the specimen. CONCLUSIONS: Neurofibromatosis with retroperitoneal stromal tumour is very rare, and radiological, pathological and immunohistochemical examination may identify it. Surgical resection may be the unique method of cure for it.

Knockout of plasminogen activator inhibitor 1 gene reduces amyloid beta peptide burden in a mouse model of Alzheimer's disease.

Accumulation of amyloid beta peptide (Aß) in the brain is a pathological hallmark of Alzheimer's disease (AD); the underlying mechanism, however, is not well understood. In this study, we show that expression of plasminogen activator inhibitor 1 (PAI-1), a physiological inhibitor of tissue type and urokinase type plasminogen activators (tPA and uPA), increases with age in the brain of wild type and Aß precursor protein-presenilin 1 (APP/PS1) transgenic mice as well as in AD patients. Most importantly, we show that knocking out the PAI-1 gene dramatically reduces Aß burden in the brain of APP/PS1 mice but has no effect on the levels of full-length APP, alpha or beta C-terminal fragments. Furthermore, we show that knocking out the PAI-1 gene leads to increases in the activities of tPA and plasmin, and the plasmin activity inversely correlates with the amounts of SDS insoluble Aß40 and Aß42. Together, these data suggest that increased PAI-1 expression/activity contributes importantly to Aß accumulation during aging and in AD probably by inhibiting plasminogen activation and thus Aß degradation.

Oxidative stress and glutathione in TGF-beta-mediated fibrogenesis.

Transforming growth factor beta (TGF-beta) is the most potent and ubiquitous profibrogenic cytokine, and its expression is increased in almost all the fibrotic diseases and in experimental fibrosis models. TGF-beta increases reactive oxygen species production and decreases the concentration of glutathione (GSH), the most abundant intracellular free thiol and an important antioxidant, which mediates many of the fibrogenic effects of TGF-beta in various types of cells. A decreased GSH concentration is also observed in human fibrotic diseases and in experimental fibrosis models. Although the biological significance of GSH depletion in the development of fibrosis remains obscure, GSH and N-acetylcysteine, a precursor of GSH, have been used in clinics for the treatment of fibrotic diseases. This review summarizes recent findings in the field to address the potential mechanism whereby oxidative stress mediates fibrogenesis induced by TGF-beta and the potential therapeutic value of antioxidant treatment in fibrotic diseases.

Dynamic distribution of Thr3-phosphorylated histone H3 in CHO cells in mitosis.

The phosphorylation of histone H3 at Ser10, Ser28, Thr11 and Thr3 of the amino terminal has been proved related to mitosis of the mammalian cells. However, the function of the Thr3 phosphorylation of H3 remains unclear. In this study, indirect immunofluorescence labelling and laser confocal microscopy were used to examine the cellular dynamic distribution of Thr3-phosphorylated H3 at mitosis in CHO cells. The results showed that the Thr3 phosphorylation began at early prophase and spread throughout the chromosomes at late prophase. At metaphase, most of the Thr3-phosphorylated H3 was distributed along the entire chromosomal arms and maintained until early anaphase. During late anaphase and telophase, the fluorescent signal of Thr3-phosphorylated H3 disappeared from chromosomes. There was a precise spatial and temporal correlation between H3 phosphorylation of Thr3 and stages of chromatin condensation. The timing of Thr3 phosphorylation and dephosphorylation in mitosis were similar to that reported for Thr11 phosphorylation of H3. The Thr3-phosphorylated H3 localized along the arms of chromosomes during metaphase and early anaphase. It was different from the Ser10-phosphorylated H3, which localized at telomere regions, and Thr11-phosphorylated H3, which localized at centromeres. The results suggest that the Thr3 phosphorylation of histone H3 may play a specific role, which is different from Ser10 phosphorylation and Thr11 phosphorylation in mitosis.