Long Noncoding RNA SNHG5 Induces the NF-KB Pathway by Regulating miR-181c-5p/CBX4 Axis to Promote the Progression of Non-Small Cell Lung Cancer

Objective: Explorations have been progressing in decoding the mechanism of non-small cell lung cancer (NSCLC). However, long noncoding RNA small nucleolar RNA host gene 5/microRNA-181c-5p/chromobox protein 4 (SNHG5/miR-181c-5p/CBX4) axis-oriented mechanisms in NSCLC is still in infancy. Therein, this study is proposed to probe this axis in NSCLC progression. Methods: Samples of 86 NSCLC patients were collected and SNHG5, miR-181c-5p and CBX4 expression was detected in NSCLC tissues and cells. NSCLC cells were transfected with plasmids to change SNHG5, miR-181c-5p or CBX4 expression, after which cell functions and phosphorylated (p)-nuclear factor (NF)-κB protein expression were evaluated. The relationships among SNHG5, miR-181c-5p and CBX4 were validated. Tumor xenografts were implemented to verify the roles of SNHG5, miR-181c-5p and CBX4 in tumor growth. Results: Low miR-181c-5p and high SNHG5 and CBX4 levels were found in NSCLC tissues and cells. Restoration of miR-181c-5p or knockdown of SNHG5 or CBX4 restrained NSCLC cell progression and inactivated the NF-κB pathway. Upregulated CBX4 abolished the effects of miR-181c-5p on reducing NSCLC cell progression. SNHG5 regulated the interaction between miR-181c-5p and CBX4. In vivo, restoration of miR-181c-5p or knockdown of SNHG5 or CBX4 retarded the tumor growth. Conclusion: This study has delineated that SNHG5 induces the NF-κB pathway by regulating the miR-181c-5p/CBX4 axis to promote NSCLC progression, which may pave a novel path for NSCLC treatment. (AU)

MiR-507 inhibits the progression of gastric carcinoma via targeting CBX4-mediated activation of Wnt/B-catenin and HIF-1α pathways

Purpose: Gastric carcinoma (GC) is a common malignant disease with high morbidity and mortality. MiR-507 has been confirmed as a tumor inhibitor which can suppress the progression of multiple cancers while its role in GC remains unknown.MethodsIn this study, the expression levels of miR-507 in the GC tissues and cells were observed by qRT-PCR, and CCK-8 assay, transwell asssay and TUNEL assay were used to observe the function of miR-507 on GC. The miRNA database and dual-luciferase reporter assay were used to investigate the downstream target of miR-507. Moreover, the activities of Wnt/β-catenin and HIF-1α pathways were observed by western blot.ResultsThe results showed that miR-507 was significantly downregulated in GC tissues and cell lines, and miR-507 upregulation effectively inhibited the proliferation and invasion and induced the apoptosis of GC cells. CBX4 was a downstream target of miR-507, and CBX4 could reverse the effects of miR-507 on the GC cells. Moreover, it was determined that miR-507 could inhibit CBX4 expression to suppress the activation of Wnt/β-catenin and HIF-1α pathways.ConclusionsIn conclusion, it suggests that miR-507 could inhibit the progression of GC via regulating CBX4-mediated activation of Wnt/β-catenin and HIF-1α pathways. (AU)

Síndrome antisintetasa / Anti-synthetase syndrome

No disponible

Different vasoactive effects of chronic endothelial and neuronal NO-synthase inhibition in young Wistar rats

While the unequivocal pattern of endothelial nitric oxide synthase (eNOS) inhibition in cardiovascular control is recognized, the role of NO produced by neuronal NOS (nNOS) remains unclear. The aim of this study was to compare the effects of chronic treatment with 7-nitroindazole (7-NI, nNOS inhibitor) and NG-nitro-l-arginine methylester (l-NAME, general and predominantly eNOS inhibitor) on cardiovascular system of young normotensive rats. Wistar rats (4 weeks old) were used: controls and rats administered either 7-NI (10 mg/kg bw/day) or l-NAME (50 mg/kg bw/day) in drinking water for 6 weeks. The systolic blood pressure (sBP) was measured by plethysmographic method, and the vasoactivity of isolated arteries was recorded. 7-NI-treatment did not affect sBP; however, the sBP was increased after l-NAME-treatment. l-NAME inhibited acetylcholine-induced relaxation of thoracic aorta (TA), whereas it remained unchanged after 7-NI-treatment. The response of TA to sodium nitroprusside was increased in both experimental groups. The expression of eNOS and nNOS in TA was unchanged in both experimental groups, whereas the activity of NOS was decreased in l-NAME-treated group. Noradrenaline- and angiotensin II-induced contractions of TA were reduced in l-NAME-treated group; however, the contractions remained unchanged in 7-NI-treated group. In all groups, the endogenous angiotensin II participated in adrenergic contraction of TA; this contribution was significantly increased in l-NAME-treated group. Neurogenic contractions in mesenteric artery (MA) remained unchanged after 7-NI-treatment, but increased after l-NAME-treatment. Results show that NO deficiency induced by administration of 7-NI and l-NAME had different cardiovascular effects: eNOS and nNOS triggered distinct signaling pathways in young normotensive rats

Síndrome por anticuerpos antisintetasa / Anti-synthetase syndrome

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Síndrome antisintetasa sin miositis con amiloidosis secundaria AA: una asociación no descrita / No disponible

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Differential toxicity of antifungal protein AFP against mutants of Fusarium oxysporum

Antifungal protein (AFP) from Aspergillus giganteus was assayed for toxicity against the Fusarium oxysporum wild-type strain and mutants in genes involved in cell signaling (DeltapacC, pacCc Deltafmk1) or cell-wall biogenesis (DeltachsV, Deltachs7, Deltagas1). The mutants were classified into two groups according to their sensitivity to AFP: DeltapacC, Deltagas1 and Deltachs7, which were significantly more resistant to AFP than the wild-type, and pacCC, Deltafmk1 and DeltachsV, which were more sensitive. Western blot analysis revealed increased binding of AFP to the three resistant mutants, DeltapacC, Deltagas1 and Deltachs7, but also to DeltachsV, indicating that differential binding may not be a key determinant for sensitivity. Addition of Ca2+ or K+ dramatically reduced antifungal activity and binding of AFP, suggesting that these cations compete for the same targets as AFP at the surface of the fungal cell (AU)

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Miopatías inflamatorias. Nuevos conceptos / Inflammatory myopathies. New concepts

Las miopatías son enfermedades caracterizadas por afectar de forma primaria al músculo esquelético. En general cursan con debilidad, dolor, contractura, calambres, rigidez o fatiga. Pueden ser hereditarias, como las miopatías distróficas, congénitas, miotónicas, metabólicas y miasténicas, o adquiridas. Entre estas últimas se incluyen las miopatías inflamatorias idiopáticas (MII), tóxicas, endocrinas o infecciosas y la miastenia gravis. Actualmente, se acepta que existe un solapamiento clínico e histopatológico considerable entre algunas distrofias musculares y algunas MII. Sin embargo, el perfil molecular del músculo es diferente y característico en cada miopatía, por lo que el estudio de los patrones de expresión de genes en el músculo puede ser útil en su diagnóstico diferencial, incluso en las MII (AU)

Myopathies are diseases characterized by the primary affection of skeletal muscle. In general they present with muscle weakness, pain, contracture, paresthesias, rigidity, or fatigue. They can be hereditary, such as muscle dystrophies, congenital, myotonic, metabolic, and myasthenic, or acquired. Among the latter ones we include idiopathic inflammatory myopathies (IIM), toxic, endocrine, or infectious myopathies and myasthenia gravis. There is a current acceptance of considerable clinical and histopathological overlap among some muscle dystrophies and some IIM. However, the molecular profile is different and characteristic in each myopathy and the study into the patterns of expression of genes in the muscle can be useful in their differential diagnosis, including that of IIM (AU)

Síndrome antisintetasa sin afectación miosítica: a propósito de un caso / Antisynthetase syndrome without myositic disease: a case report

El síndrome antisintetasa (SAS) es un trastorno infrecuente, incluido entre las miopatías inflamatorias idiopáticas, que se caracteriza por la presencia de anticuerpos antisintetasa (ACAS). Presentamos el caso de un paciente con cuadro clínico consistente en afectación intersticial pulmonar,alteraciones cutáneas y articulares, pero sin afectación muscular, junto con la presencia de anticuerpos anti-Jol

Antisynthetase syndrome is a rare disorder, included among the idiopathic inflammatory myopathies, characterized by the presence of antisynthetase antibodies. We present a case of a patient with a sugestive clinical stage of interstitial lung disease, skin and articular disease, but without muscle involvement, with the presence of anti Jol antibodies

Síndrome antisintetasa y afección pulmonar intersticial. Descripción de 6 casos / Antisynthetase syndrome and interstitial lung involvement. Report of 6 cases

Presentamos los casos de 6 pacientes, 4 varones y 2 mujeres, diagnosticados de síndrome antisintetasa con afección pulmonar. La edad media era de 60 años. El síntoma guía desde el punto de vista respiratorio fue la disnea progresiva, presente en 4 pacientes. De los otros dos pacientes, uno tenía hemoptisis y el otro estaba asintomático. Respecto a la clínica sistémica, 2 pacientes presentaban fenómeno de Raynaud, 3 artritis de manos y 4 afección muscular. La radiografía del tórax revelaba la presencia de infiltrados intersticiales lineales de distinto grado en todos los casos menos en un paciente, quien además padecía una silicosis. La exploración funcional respiratoria demostró una alteración ventilatoria restrictiva en 4 casos, de carácter obstructivo en un paciente afectado de EPOC y normal en otro. El anticuerpo antisintetasa (ACAS) detectado fue el anti-Jo1 en 4 casos y el anti-PL12 en otro. En el sexto caso no se determinó la naturaleza del ACAS. La evolución de los enfermos fue favorable en todos los casos menos en uno. La determinación de los ACAS es de utilidad dentro del estudio de las neumopatías intersticiales idiopáticas (AU)

Genética de la enfermedad de Parkinson / Genetics and Parkinson disease

No disponible