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Circular RNAs (circRNAs) are increasingly gaining importance and attention due to their diverse potential functions and their value as diagnostic biomarkers (disease specific). This study aims to explore the novel mechanisms by which exosome-contained circRNAs promote tumor development and metastasis in TNBC. We identified increased circRNA circPSMA1 in TNBC cells, their exosomes, and serum exosomes samples from TNBC patients. The overexpression of circPSMA1 promoted TNBC cell proliferation, migration, and metastasis both in vitro and in vivo. Moreover, we investigated the tumor-infiltrating immune cells (TICs) or stromal components in immune microenvironment (IME), and identified the significant differences in the immune cells between TNBC and non-TNBC samples. Mechanistically, circPSMA1 acted as a “miRNAs sponge” to absorb miR-637; miR-637 inhibited TNBC cell migration and metastasis by directly targeted Akt1, which recognized as a key immune-related gene and affected downstream genes β-catenin and cyclin D1. Subsequent co-culture experiments also demonstrated that exosomes from TNBC carrying large amounts of circPSMA1 could transmit migration and proliferation capacity to recipient cells. Kaplan–Meier plots showed that high expression of Akt1 and low expression of mir-637 are highly correlated with poor prognosis in patients with lymph node metastasis of TNBC. Collectively, all these results reveal that circPSMA1 functions as a tumor promoter through the circPSMA1/miR-637/Akt1-β-catenin (cyclin D1) regulatory axis, which can facilitate the tumorigenesis, metastasis, and immunosuppression of TNBC. Our research proposes a fresh perspective on novel potential biomarkers and immune treatment strategies for TNBC.

Background More initial clinical node‐positive breast cancer patients achieve axillary pathological complete response (ax‐pCR) after neoadjuvant systemic therapy (NST). Restaging axillary status and performing de‐escalated surgical procedures to replace routine axillary lymph nodes dissection (ALND) is urgently needed. Targeted axillary lymph node biopsy (TLNB) is a novel de‐escalated surgical strategy marking metastatic axillary nodes before NST and targeted dissection and biopsy intraoperatively to tailor individual axillary management. Methods This study provided a systematic review and meta‐analysis to evaluate the feasibility and diagnosis accuracy of TLNB. Prospective and retrospective clinical trials on TLNB were searched from Pubmed, Embase, and Cochrane. Identification rate (IFR), false‐negative rate (FNR), negative predictive value (NPV), and rate of ax‐pCR were the outcomes of this meta‐analysis. Results One thousand nine hundred and twenty patients attempted TLNB, with an overall IFR of 93.5% (95% confidence interval [CI] 90.1%–96.2%). IFR of three nodal marking methods, namely iodine seeds, clips, and carbon dye, was 95.6% (95% CI 91.2%–98.7%), 91.7% (95% CI 87.3%–95.4%), and 97.1% (95% CI 89.1%–100.0%), respectively. Of them, 847 patients received ALND, with an overall FNR of 5.5% (95% CI 3.3%–8.0%), and NPV ranged from 90.1% to 96.1%. Regression analysis showed that the overlap of targeted and sentinel biopsied nodes might associate with IFRs and FNRs. Conclusion TLNB is a novel, less invasive surgical approach to distinguish initial node‐positive breast cancer that achieves negative axillary conversion after NST. It yields an excellent IFR with a low FNR and a high NPV. A combination of preoperative imaging, intraoperative TLNB with SLNB, and postoperative nodal radiotherapy might affect the future treatment paradigm of primary breast cancer with nodal metastases. Axillary surgeries for node‐positive neoadjuvant breast cancer could be de‐escalated. Targeted lymph node dissection has high feasibility and diagnosis accuracy. A stepwise treatment strategy combining imaging and radiotherapy is recommended.

MiRNAs, small non-coding RNA molecules, were recognized to be associated with the incidence and development of diverse neoplasms. MiRNAs were small non-coding RNAs that could regulate post-transcriptional level by binding to 3′-UTR of target mRNAs. Amongst which, miR-29a was demonstrated that it had significant impact on oncogenicity in various neoplasms through binding to critical genes which enhanced or inhibited the progression of cancers. MiR-29a participated in kinds of physiological and pathological processes, including virus replication, cell proliferation, differentiation, apoptosis, fibrosis, angiogenesis, tumorigenicity, metastasis, drug-resistance, and so on. According to its sufficient sensitivity and specificity, many studies showed that miR-29a might serve as a potential therapeutic target and promising biomarker in various tumors. In this review, we discussed the functions of miR-29a and its potential application in the diagnosis, treatment and stages of carcinoma, which could provide additional insight to develop a novel therapeutic strategy.

To study the role of hsa_circ_0072995 in regulating the invasion and migration of breast cancer cells. Hsa_circ_0072995 expression was confirmed by quantitative real-time PCR; evaluating the migration and invasion of breast cancer cells through transwell assay; predicating circRNA/microRNAs interaction using the miRanda and RNAhybrid software; identifying the relationship between hsa_circ_0072995 and miR-30c-2-3p by luciferase activity assay; detecting the location of hsa_circ_0072995 by Fluorescence hybridization assay. Hsa_circ_0072995 was significantly upregulated in MDA-MB-231 cells compared with MCF-7 cells. Hsa_circ_0072995 regulated the invasion and migration of breast cancer cells. Hsa_circ_0072995 existed in the nucleus and cytoplasm, and the proportion of the two was roughly equal. Hsa_circ_0072995 bound to miR-30c-2-3p. Overexpression of miR-30c-2-3p inhibited breast cancer cells migration and invasion. Low expression of miR-30c-2-3p was correlated with poor overall survival by The Cancer Genome Atlas database. Hsa_circ_0072995 may be a novel biomarker for breast cancer, and may function in metastasis of breast cancer.

Circular RNAs (circRNAs) are a unique family of noncoding RNAs that could regulate multiple biological processes, which play a crucial role in carcinogenesis, progression and chemotherapy resistance of cancers. Growing studies have demonstrated that circRNAs act as novel biomarkers and therapeutic targets for cancers by sponging microRNAs (miRNAs). Up to date, another function of circRNAs, combining with RNA-binding proteins (RBPs), was uncovered. However, there is limit studies illustrating the underlying mechanism of circRNAs-RBPs interactions, as well as showing its roles in diverse types of cancers. In this review, we collected the biogenesis, properties of circRNAs, and then synthesize the connection between circRNAs and RBPs, and try to clarify its molecular mechanisms involving in the pathogenesis and progression of several common cancers, aiming to provide a brand-new insight to the prognosis and treatment strategy for cancers.

Exosomes are small membrane vesicles with a diameter of 40-100 nm, which are released into the intracellular environment. Exosomes could influence the genetic and epigenetic changes of receptor cells by promoting the horizontal transfer of various proteins or RNAs, especially miRNAs. Moreover, exosomes also play an important role in tumor microenvironment. Exosomes could promote the short- and long-distance exchanges of genetic information by acting as mediators of cell-to-cell communication. In addition, exosomes participate in drug resistance of tumor cells by genetic exchange between cells. It is reported that exosomes could be absorbed by recipient cells and transmit chemoresistance from drug-resistant tumor cells to sensitive ones. Then understanding the mechanisms of chemotherapy failure and controlling tumor progression effectively will be a major challenge for us. Therefore, in this review, we will briefly reveal the role of exosomes in drug resistance.

The study aimed to investigate the role of circular RNA circASS1 in breast cancer cells. Circular RNAs microarray expression profile were analyzed in MCF-7, MDA-MB-231, and qRT-PCR and western blotting were used to quantify expression of circASS1 and its parental gene . Wound healing, migration and invasion assay were performed. Luciferase assay system was used to detect harbored miRNA. CircASS1 in MDA-MB-231 is downregulated comparing to MCF-7, and overexpression of circASS1 could suppress invasion and migration. While silence, it could promote invasion and migration. MiR-4443 functioning as a tumor promoter gene could be captured by circASS1. ASS1 is upregulated in loss-of-function experiments, while downregulated in gain-of-function experiments. CircASS1 suppresses invasion and migration capacity of breast cancer cells and harbored miR-4443.

Unmanned helicopters equipped with adaptive landing gear will dramatically extend their application especially in dealing with challenging terrains. This study presents a novel cable-driven legged landing gear (CLG) with differential transmission for unmanned helicopters in complex landing environments. To obtain the preferred configuration of the legged mechanism, a multi-objective optimization framework for the CLG is constructed by concurrently considering terrain adaptability, landing stability and reasonable linkage of internal forces. The non-dominated sorting genetic algorithm II is employed to numerically acquire the optimal scale parameters that guide the mechanical design of the CLG. An unmanned helicopter prototype equipped with the devised CLG is developed with key performance assessment. Experimental results show that the devised CLG can provide energy-efficient support over uneven terrains (totally driven torque demand less than 0.1 N m) in quasi-static landing tests, and favorable terrain adaptability (posture fluctuation of the fuselage less than ±1°) in unknown slope landing tests. These exhibited merits give the proposed CLG the potential to enhance the landing performance of future aircraft in extreme environments.

To enhance the microwave absorption performance of silicon carbide nanowires（SiCNWs）, SiO2 nanoshells with a thickness of approximately 2 nm and Fe3O4 nanoparticles were grown on the surface of SiCNWs to form SiC@SiO2@Fe3O4 hybrids. The microwave absorption performance of the SiC@SiO2@Fe3O4 hybrids with different thicknesses was investigated in the frequency range from 2 to 18 GHz using a free-space antenna-based system. The results indicate that SiC@SiO2@Fe3O4 hybrids exhibit improved microwave absorption. In particular, in the case of an SiC@SiO2 to iron（III） acetylacetonate mass ratio of 1:3, the microwave absorption with an absorber of 2-mm thickness exhibited a minimum reflection loss of-39.58 d B at 12.24 GHz. With respect to the enhanced microwave absorption mechanism, the Fe3O4 nanoparticles coated on SiC@SiO2 nanowires are proposed to balance the permeability and permittivity of the materials, contributing to the microwave attenuation.

Aim： To study whether epigallocatechin gallate （EGCG）, a green tea-derived polyphenol, exerted anti-influenza A virus activity in vitro and in vivo. Methods： Madin-Darby canine kidney （MDCK） cells were tested. The antiviral activity of EGCG in the cells was determined using hemagglutination assay and qPCR. Time of addition assay was performed to determine the kinetics of inhibition of influenza A by EGCG. The level of reactive oxygen species （ROS） were determined with confocal microscopy and flow cytometry. BALB/c mice were treated with EGCG （10, 20 or 40 mg·kg-l·d-1, pc） for 5 d. On the 3rd d of the treatment, the mice were infected with influenza A virus. Histopathological changes, lung index and virus titers in the lungs were determined. Results： Treatment of influenza A-infected MDCK cells with EGCG （1.25-100 nmol/L） inhibited influenza A replication in a concen- tration-dependent manner （the EDso value was 8.71±1.11 nmol/L）. Treatment with EGCG （20 nmol/L） significantly suppressed the increased ROS level in MDCK cells following influenza A infection. In BALB/c mice infected with influenza virus, oral administration of EGCG （40 mg·kg-1·d-1） dramatically improved the survival rate, decreased the mean virus yields and mitigated viral pneumonia in the lungs, which was equivalent to oral administration of oseltamivir （40 mg·kg-1·d-1）, a positive control drug. Conclusion： The results provide a molecular basis for development of EGCG as a novel and safe chemopreventive agent for influenza A infection.