0D van der Waals interfacial ferroelectricity.

The dimensional limit of ferroelectricity has been long explored. The critical contravention is that the downscaling of ferroelectricity leads to a loss of polarization. This work demonstrates a zero-dimensional ferroelectricity by the atomic sliding at the restrained van der Waals interface of crossed tungsten disufilde nanotubes. The developed zero-dimensional ferroelectric diode in this work presents not only non-volatile resistive memory, but also the programmable photovoltaic effect at the visible band. Benefiting from the intrinsic dimensional limitation, the zero-dimensional ferroelectric diode allows electrical operation at an ultra-low current. By breaking through the critical size of depolarization, this work demonstrates the ultimately downscaled interfacial ferroelectricity of zero-dimensional, and contributes to a branch of devices that integrates zero-dimensional ferroelectric memory, nano electro-mechanical system, and programmable photovoltaics in one.

Erratum: [Corrigendum] MicroRNA­23a inhibits endometrial cancer cell development by targeting SIX1.

[This corrects the article DOI: 10.3892/ol.2019.10694.].

Rapid Production of Carbon Nanotube Film for Bioelectronic Applications.

Flexible electronics have enormous potential for applications that are not achievable in standard electronics. In particular, important technological advances have been made in terms of their performance characteristics and potential range of applications, ranging from medical care, packaging, lighting and signage, consumer electronics, and alternative energy. In this study, we develop a novel method for fabricating flexible conductive carbon nanotube (CNT) films on various substrates. The fabricated conductive CNT films exhibited satisfactory conductivity, flexibility, and durability. The conductivity of the conductive CNT film was maintained at the same level of sheet resistance after bending cycles. The fabrication process is dry, solution-free, and convenient for mass production. Scanning electron microscopy revealed that CNTs were uniformly dispersed over the substrate. The prepared conductive CNT film was applied to collect an electrocardiogram (ECG) signal, which showed good performance compared to traditional electrodes. The conductive CNT film determined the long-term stability of the electrodes under bending or other mechanical stresses. The well-demonstrated fabrication process for flexible conductive CNT films has great potential in the field of bioelectronics.

Mesoscopic sliding ferroelectricity enabled photovoltaic random access memory for material-level artificial vision system.

Intelligent materials with adaptive response to external stimulation lay foundation to integrate functional systems at the material level. Here, with experimental observation and numerical simulation, we report a delicate nano-electro-mechanical-opto-system naturally embedded in individual multiwall tungsten disulfide nanotubes, which generates a distinct form of in-plane van der Waals sliding ferroelectricity from the unique combination of superlubricity and piezoelectricity. The sliding ferroelectricity enables programmable photovoltaic effect using the multiwall tungsten disulfide nanotube as photovoltaic random-access memory. A complete "four-in-one" artificial vision system that synchronously achieves full functions of detecting, processing, memorizing, and powering is integrated into the nanotube devices. Both labeled supervised learning and unlabeled reinforcement learning algorithms are executable in the artificial vision system to achieve self-driven image recognition. This work provides a distinct strategy to create ferroelectricity in van der Waals materials, and demonstrates how intelligent materials can push electronic system integration at the material level.

LINC01133 and LINC01243 are positively correlated with endometrial carcinoma pathogenesis.

PURPOSE: To characterize the role of two long non-coding RNAs (lncRNAs), LINC01133 and LINC01243, in endometrial carcinoma (EC) pathogenesis. LINC01133 is an lncRNA that has been implicated in many cancers, and LINC01243 is a newly identified lncRNA identified from the NCBI GEO database. METHODS: We studied the effect of LINC01133 and LINC01243 on EC malignancy using siRNA knockdown and real-time quantitative polymerase chain reaction (RT-qPCR), flow cytometry, Annexin V-FITC/propidium iodide double staining, Transwell, and scratch invasion assays in two EC cell lines (Ishikawa and HEC-1-A cells). RESULTS: We first confirmed the partial knockdown of both LINC01133 and LINC01243 expression in Ishikawa and HEC-1-A cells using RT-qPCR. Following confirmation of lncRNA knockdown, we assessed the effect of knockdown on EC malignancy. We observed reduced EC cell proliferation using the CCK-8 assay, as well as cell cycle arrest and increased apoptosis in both EC cell lines. Furthermore, Transwell and scratch invasion assays revealed decreased migration and invasion of the two EC cell lines, respectively. CONCLUSION: We demonstrated that LINC01133 and LINC01243 expression are associated with EC development and progression. Our findings suggest a potential role for these lncRNAs as novel EC biomarkers.

CYPA promotes the progression and metastasis of serous ovarian cancer (SOC) in vitro and in vivo.

Ovarian cancer (OC) is a type of gynaecological malignancy with high mortality in females. Serous ovarian cancer (SOC) is a distinct subtype of OC with poor early diagnosis. Given the limitations of traditional therapies, such as chemotherapy, targeted treatment is therefore a promising therapy to improve the survival rate of SOC patients. Cyclophilin A (CYPA) is a member of Cyclophilin family and thought to participates in multiple cellular processes such as cell transduction and immune modulation. Recently, various of studies indicated that CYPA has critical impact on cancer progression. CYPA could regulate cell proliferation, invasion, and chemoresistance of multiple types of cancers. However, it is still unclear whether it could affect ovarian cancer. In this study, we demonstrated that CYPA was highly expressed in SOC tissues compared with adjacent tissues. Further, CYPA was significantly associated with clinical stage and lymphnode metastasis of SOC patients. Additionally, data indicated that knockdown of CYPA by its shRNA dramatically reduces migration and invasion capacity of SOC cells in vitro and blocks tumor metastasis in vivo. Our study investigates the involvement of CYPA in the progression and metastasis of SOC, and therefore provides CYPA as a promising therapeutic target for SOC treatment.

MicroRNA-23a inhibits endometrial cancer cell development by targeting SIX1.

The present study focused on exploring the inhibitory mechanism of microRNA (miR)-23a in endometrial cancer. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to investigate miR-23a expression in endometrial tissues and endometrial cancer cells. A colony formation assay using crystal violet staining was performed to compare cell proliferation, while wound-healing and Transwell assays were performed to compare cell migration and invasion. Subsequently, bioinformatics and a luciferase reporter gene assay were used to investigate the effect of miR-23a on sine oculis homeobox homolog 1 (SIX1) expression, and the biological function of SIX1 was analyzed. Additionally, a nude mouse tumorigenicity assay was performed to test the inhibitory effect of miR-23a and Taxol® therapy in endometrial cancer. Finally, immunohistochemistry and RT-qPCR were used to explore the association between miR-23a and SIX1 expression in endometrial cancer tissues. miR-23a was underexpressed in endometrial cancer tissues compared with in para-carcinoma tissues, and the overexpression of miR-23a inhibited proliferation and invasion of endometrial cancer cells. Furthermore, SIX1 was demonstrated to be a downstream target of miR-23a, and miR-23a reduced SIX1 expression. Additionally, SIX1 inversely promoted cell proliferation, migration and invasion. In addition, the effects of reduced cell proliferation and increased cell invasion following miR-23a overexpression could be reversed by adding SIX1 to in vitro culture. Furthermore, the inhibitory effect of miR-23a and Taxol therapy, which reduced SIX1 expression in endometrial cancer, was demonstrated in vivo. Finally, a negative association between miR-23a and SIX1 expression was demonstrated in endometrial cancer tissues. The results of the present study revealed that miR-23a may inhibit endometrial cancer development by targeting SIX1.

MiR-155-5p inhibits PDK1 and promotes autophagy via the mTOR pathway in cervical cancer.

Cervical cancer is one of the most common malignant tumors and the leading cause of cancer-related mortality in women. Persistent cervical infection by high-risk human papillomavirus (hrHPV) is related to cervical cancer. MicroRNAs could regulate autophagy caused by viral infection. The aim of the present study was to investigate the regulation of autophagy by miR-155-5p in cervical cancer. In HPV+ human cervical lesion tissues, miR-155-5p expression was found to be markedly decreased. Compared to C33A cancer cells (HPV-), the miR-155-5p expression was significantly lower in Siha and HeLa cells (HPV+), which are both hrHPV positive. The level of autophagy was higher in C33A cells than in Siha and HeLa cells. In addition, in C33A, Siha and HeLa cervical cancer cells, miR-155-5p overexpression promoted autophagy, whereas miR-155-5p downregulation had the opposite effects. Furthermore, miR-155-5p downregulation suppressed LC3 and promoted P62 protein expression in C33A cells through promoting the PDK1/mTOR pathway, whereas miR-155-5p overexpression recovered LC3 and suppressed P62 protein expression by suppressing PDK1/mTOR signaling. Taken together, our results indicate the importance of miR-155-5p in cervical cancer cells and suggest a novel mechanism of hrHPV in promoting cervical lesions.

Pegylated liposomal­paclitaxel induces ovarian cancer cell apoptosis via TNF­induced ERK/AKT signaling pathway.

Ovarian cancer is one of the most common gynecological types of cancer and is characterized by a relatively high incidence and high mortality rate. Evidence has demonstrated that paclitaxel (PTX) is an effective therapeutic treatment for human ovarian cancer. In the present study, the inhibitory effects of pegylated liposomal (PL)­PTX on the growth of ovarian cancer cells were investigated in vitro; a CAOV­3­bearing mouse model was established to investigate the in vivo effects of PL­PTX on ovarian tumor growth. In the present study, the underlying mechanism of tumor necrosis factor (TNF)­induced inhibition of extracellular signal­regulated kinase (ERK)/protein kinase B (AKT) signaling pathway mediated by PL­PTX was analyzed within ovarian cancer cells. The results of the present study revealed that PL­PTX significantly inhibited the growth and aggressiveness of ovarian cancer cells in vitro and in vivo and apoptotic ability increased upon administration of PL­PTX. The expression levels of caspase­3/9 were significantly upregulated within PL­PTX­treated ovarian cancer cells. The expression and phosphorylation levels of ERK and AKT were markedly increased in response to PL­PTX treatment. In addition, the inhibitory effects of PL­PTX on ovarian cancer cells were eliminated by neutralizing antibodies against TNF. The observations of the present study revealed that PL­PTX induced ovarian cell apoptosis via the TNF­dependent pathway, which was significantly inhibited with the employment of antibodies against TNF. In vivo analysis demonstrated that PL­PTX treatment significantly inhibited ovarian tumor growth and prolonged the survival of tumor bearing mice. In conclusion, the findings of the present study have provided an insight into the potential mechanism of PL­PTX­induced apoptosis of ovarian cancer cells. As PL­PTX has been reported to induce ovarian tumor cell apoptosis via the TNF­induced ERK/AKT signaling pathway, PL­PTX may serve as an efficient anticancer drug for the treatment of ovarian cancer.