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In the past several decades, Photoelectrochemical (PEC) sensing still remains a great challenge to design highly-efficient semiconductor photocatalysts via a facile method. It is of much importance to design and synthesize various novel nanostructured sensing materials for further improving the response performance. Herein, we present an In2 O3 /In2 S3 heterostructure obtained by combining microwave assisted hydrothermal method with S-induced phase change, whose energy band and electronic structure could be adjusted by changing the S content. Combining theoretical calculation and spectroscopic techniques, the introduction of sulfur was proved to produce multifunctional interfaces, inducing the change of phase, oxygen vacancies and band gap, which accelerates the separation of photoexcited carriers and reduces their recombination, improving the electronic injection efficiency around the interface of In2 O3 /In2 S3 . As anticipated, an enhanced glucose response performance with a photocurrent of 0.6â mA cm-2 , a linear range of 0.1-1â mM and a detection limit as low as 14.5â µM has been achieved based on the In2 O3 /In2 S3 heterostructure, which is significant superior over its pure In2 O3 and S-doped In2 O3 counterparts. This efficient interfacial strategy may open a new route to manipulate the electrical structure, and energy band structure regulation of sensing material to improve the performance of photoelectrodes for PEC.
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The Hox transcript antisense intergenic RNA (HOTAIR) has been identified as a tumor gene, and its expression in HCC is significantly increased. HOTAIR is associated with the proliferation, invasion, metastasis and poor prognosis of HCC. In addition, HOTAIR can also regulate the expression and function of microRNA by recruiting the polycomb repressive complex 2 (PRC2) and competitive adsorption, thus promoting the occurrence and development of HCC. In this review, we discussed the two mechanisms of HOTAIR regulating miRNA through direct binding miRNA and indirect regulation, and emphasized the role of HOTAIR in HCC through miRNA, explained the regulatory pathway of HOTAIR-miRNA-mRNA and introduced the role of this pathway in HCC proliferation, drug resistance, invasion and metastasis.
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Interactions between the mitochondrial inner and outer membranes and between mitochondria and other organelles closely correlates with the sensitivity of ovarian cancer to cisplatin and other chemotherapeutic drugs. However, the underlying mechanism remains unclear. Recently, the mitochondrial protease OMA1, which regulates internal and external signals in mitochondria by cleaving mitochondrial proteins, was shown to be related to tumor progression. Therefore, we evaluated the effect of OMA1 on the response to chemotherapeutics in ovarian cancer cells and the mouse subcutaneous tumor model. We found that OMA1 activation increased ovarian cancer sensitivity to cisplatin in vivo and in vitro. Mechanistically, in ovarian cancer, OMA1 cleaved optic atrophy 1 (OPA1), leading to mitochondrial inner membrane cristae remodeling. Simultaneously, OMA1 induced DELE1 cleavage and its cytoplasmic interaction with EIF2AK1. We also demonstrated that EIF2AK1 cooperated with the ER stress sensor EIF2AK3 to amplify the EIF2S1/ATF4 signal, resulting in the rupture of the mitochondrial outer membrane. Knockdown of OMA1 attenuated these activities and reversed apoptosis. Additionally, we found that OMA1 protease activity was regulated by the prohibitin 2 (PHB2)/stomatin-like protein 2 (STOML2) complex. Collectively, OMA1 coordinates the mitochondrial inner and outer membranes to induce ovarian cancer cell death. Thus, activating OMA1 may be a novel treatment strategy for ovarian cancer.
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Estrés del Retículo Endoplásmico/fisiología , Metaloendopeptidasas/metabolismo , Mitocondrias/metabolismo , Proteínas Mitocondriales/metabolismo , Neoplasias Ováricas/metabolismo , Prohibitinas/metabolismo , Transducción de Señal/fisiología , Animales , Apoptosis/fisiología , Línea Celular , Línea Celular Tumoral , Citosol/metabolismo , Retículo Endoplásmico/metabolismo , Femenino , Humanos , Ratones , Membranas Mitocondriales/metabolismoRESUMEN
NiCo2O4 nanospheres, a type of conjugated reduced graphene oxide (rGO), are compounded by a simple and easy synthesis of Cu2O/GO and fabricated NiCo2O4/rGO nanocomposites based on a Cu2O/GO template. The structure and morphology of the hierarchical NiCo2O4/rGO are characterized by x-ray diffraction, x-ray photoelectron spectroscopy, scanning electron microscopy, and transmission electron microscopy. The electrochemistry properties of NiCo2O4/rGO composites toward glucose are determined based on a glassy carbon electrode, and the results indicate that the hollow nanospheres of NiCo2O4/rGO could achieve high-sensitivity detections of glucose. The NiCo2O4/rGO composite has a detection range of 0.04 mM to 1.28 mM, a sensitivity of 2082.57 µA mM-1 cm-2, and a detection limit of 0.7 µM. The composite further exhibits obvious stability, superior reproducibility, and excellent selectivity. This study demonstrates that NiCo2O4/rGO is a unique and material with high potential in glucose sensing.
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A photoelectrochemical (PEC) detection platform was built based on the branched rutile/anatase titanium dioxide (RA-TiO2) electrode. Theoretical calculations proved that the type-II band alignment of rutile and anatase could facilitate charge separation in the electrode. The self-generated electric field at the interface of two phases can enhance the electron transfer efficiency of the electrode. Carboxylated CdTe quantum dots (QDs) were applied as signal amplification factors. Without the target DNA presence, the CdTe QDs were riveted to the surface of the electrode by the hairpin probe DNA. The sensitization of CdTe QDs increased the photocurrent of the electrode significantly. When the target DNA was present, the structural changes of the hairpin probe DNA resulted in the failure of the sensitized structure. Benefiting from excellent electrode structure design and CdTe QDs sensitization strategy, the PEC assays could achieve highly sensitive and specific detection of target DNA in the range of 1 fM to 1 nM, with a detection limit of 0.23 fM. The electrode construction method proposed in this article can open a new avenue for the preparation of more efficient PEC sensing devices.
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Técnicas Biosensibles , Compuestos de Cadmio , Puntos Cuánticos , Compuestos de Cadmio/química , Electrones , Puntos Cuánticos/química , Telurio/química , ADN/química , Técnicas Biosensibles/métodos , Electrodos , Técnicas Electroquímicas/métodos , Límite de DetecciónRESUMEN
LncRNA HOTAIR play important roles in the epigenetic regulation of carcinogenesis and progression in liver cancer. Previous studies suggest that the overexpression of HOTAIR predicts poor prognosis. In this study, through transcriptome sequencing data and in vitro experiments, we found that HOTAIR were more highly expressed and there is significantly positive relationship between HOTAIR and NUAK1 in liver cancer tissues and cell lines. miR-145-5p was downregulated and showed negative correlation with HOTAIR and NUAK1. Transfect Sh-HOTAIR, LZRS-HOTAIR, miR-145 mimic, miR-145 inhibitor to change the expression of HOTAIR and miR-145-5p. The addition of HTH-01-015 inhibits the expression of NUAK1. HOTAIR knockdown, miR-145-5p upregulation and NUAK1 inhibition all repressed migration, invasion and metastasis and reversed the epithelial-to-mesenchymal transition in SNU-387 and HepG2 cells. We also showed that HOTAIR recruiting and binding PRC2 (EZH2) epigenetically represses miR-145-5p, which controls the target NUAK1, thus contributing to liver cancer cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with miR-145-5p/NUAK1 during epigenetic regulation. Our findings indicate that HOTAIR/miR-145-5p/NUAK1 axis acts as an EMT regulator and may be candidate prognostic biomarker and targets for new therapies in liver cancer.
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Cardiovascular disease (CVD) is considered one of the leading causes of death worldwide. In recent years, this research area has attracted researchers' attention to investigate heart sounds to diagnose the disease. To effectively distinguish heart valve defects from normal heart sounds, adaptive empirical mode decomposition (EMD) and feature fusion techniques were used to analyze the classification of heart sounds. Based on the correlation coefficient and Root Mean Square Error (RMSE) method, adaptive EMD was proposed under the condition of screening the intrinsic mode function (IMF) components. Adaptive thresholds based on Hausdorff Distance were used to choose the IMF components used for reconstruction. The multidimensional features extracted from the reconstructed signal were ranked and selected. The features of waveform transformation, energy and heart sound signal can indicate the state of heart activity corresponding to various heart sounds. Here, a set of ordinary features were extracted from the time, frequency and nonlinear domains. To extract more compelling features and achieve better classification results, another four cardiac reserve time features were fused. The fusion features were sorted using six different feature selection algorithms. Three classifiers, random forest, decision tree, and K-nearest neighbor, were trained on open source and our databases. Compared to the previous work, our extensive experimental evaluations show that the proposed method can achieve the best results and have the highest accuracy of 99.3% (1.9% improvement in classification accuracy). The excellent results verified the robustness and effectiveness of the fusion features and proposed method.
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Ruidos Cardíacos , Válvulas CardíacasRESUMEN
In recent years, more and more research is being conducted on microRNAs and their involvement in the regulation of autophagy phagocytosis which is closely related to tumor growth. MicroRNA-21 is a kind of small RNA that can regulate gene expression and plays a significant role in autophagy of tumor cells. But the detection of microRNAs had always been a problem in the field of biological analysis. In this study, we designed a new fluorescent sensor for the detection of miRNA-21. The sensor was based on the successful signal reporting by E36-encapsulated vesicles and the specific interaction between E36 and miRNA-21. In the presence of miRNA, the E36/miRNA-21 complex formed and served as a donor molecule inside the acceptor PDA vesicles to amplify the fluorescence through FRET. Additionally, the sensor was applied to detect miRNA-21 in complex biological samples with satisfactory results.
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Técnicas Biosensibles , MicroARNs , Neoplasias Ováricas , Biomimética , Femenino , Transferencia Resonante de Energía de Fluorescencia , Humanos , MicroARNs/genética , Neoplasias Ováricas/genéticaRESUMEN
OBJECTIVE: Beclin1 plays a central role in the activation of the autophagy signaling pathway. Beclin1 and LC3-related proteins are involved in the initial steps of autophagy, which are closely related to the occurrence and development of tumors. The current meta-analysis aimed to clarify the correlation between expression of Beclin1 and LC3 and prognosis of ovarian cancer. METHODS: We searched PubMed, Embase, The Cochrane Library, Web of Science, and CNKI using predefined selection criteria. Pooled hazard ratios and relative risks with 95% confidence intervals were used to evaluate the correlation between autophagy-related genes Beclin1 and LC3 and overall survival (OS), progression-free survival (PFS), and International Federation of Gynecology and Obstetrics (FIGO) stage. RESULTS: In total, 1497 patients from 10 articles were enrolled in this meta-analysis. Expression of Beclin1 was significantly correlated with improved OS and PFS, and increased expression of Beclin1 was correlated with early FIGO stage, but not with lymph node metastasis or histological grade. No association was found between LC3 expression and prognosis in patients with ovarian cancer. CONCLUSIONS: Expression of Beclin1 is an independent risk factor for the progression of ovarian cancer. Thus, Beclin1 is a promising indicator in predicting prognosis in patients with ovarian cancer.
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Neoplasias Ováricas , Autofagia , Beclina-1/genética , Carcinoma Epitelial de Ovario , Femenino , Humanos , Neoplasias Ováricas/diagnóstico , Neoplasias Ováricas/genética , PronósticoRESUMEN
Thiocoraline, a depsipeptide bisintercalator with potent antitumor activity, was first isolated from marine actinomycete Micromonospora marina. It possesses an intense toxicity to MCF-7 cells at nanomolar concentrations in a dose-dependent manner evaluated by MTT assay and crystal violet staining. We established a human breast thiocoraline-resistant cancer subline of MCF-7/thiocoraline (MCF-7/T) to investigate the expression variation of breast cancer resistance proteins (BCRP) and its subsequent influence on drug resistance. Colony-forming assay showed that the MCF-7 cells proliferated faster than the MCF-7/T cells in vitro. Western blot analysis demonstrated that thiocoraline increased the phosphorylation of Akt. Additionally, the sensitivity of tumor cells to thiocoraline was reduced with a concurrent rise in phosphorylation level of Akt and of BCRP expression.These studies indicated that thiocoraline probably mediated the drug resistance via PI3K/Akt/BCRP signaling pathway. MK-2206 dihydrochloride, a selective phosphorylation inhibitor of Akt, significantly decreased MCF-7 cell viability under exposure to thiocoraline compared to the control. However, it was not obviously able to decrease MCF-7/T cell viability when cells were exposed to thiocoraline.
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Autophagy is a "self-degradative" process and is involved in the maintenance of cellular homeostasis and the control of cellular components by facilitating the clearance or turnover of long-lived or misfolded proteins, protein aggregates, and damaged organelles. Autophagy plays a dual role in cancer, including in tumor progression and tumor promotion, suggesting that autophagy acts as a double-edged sword in cancer cells. Liver cancer is one of the greatest leading causes of cancer death worldwide due to its high recurrence rate and poor prognosis. Especially in China, liver cancer has become one of the most common cancers due to the high infection rate of hepatitis virus. In primary liver cancer, hepatocellular carcinoma (HCC) is the most common type. Considering the perniciousness and complexity of HCC, it is essential to elucidate the function of autophagy in HCC. In this review, we summarize the physiological function of autophagy in cancer, analyze the role of autophagy in tumorigenesis and metastasis, discuss the therapeutic strategies targeting autophagy and the mechanisms of drug-resistance in HCC, and provide potential methods to circumvent resistance and combined anticancer strategies for HCC patients.