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Transport through the cell membrane can be divided into active, passive and vesicular types (exosomes). Exosomes are nano‐sized vesicles released by a variety of cells. Emerging evidence shows that exosomes play a critical role in cancers. Exosomes mediate communication between stroma and cancer cells through the transfer of nucleic acid and proteins. It is demonstrated that the contents and the quantity of exosomes will change after occurrence of cancers. Over the last decade, growing attention has been paid to the role of exosomes in the development of breast cancer, the most life‐threatening cancer in women. Breast cancer could induce salivary glands to secret specific exosomes, which could be used as biomarkers in the diagnosis of early breast cancer. Exosome‐delivered nucleic acid and proteins partly facilitate the tumorigenesis, metastasis and resistance of breast cancer. Exosomes could also transmit anti‐cancer drugs outside breast cancer cells, therefore leading to drug resistance. However, exosomes are effective tools for transportation of anti‐cancer drugs with lower immunogenicity and toxicity. This is a promising way to establish a drug delivery system. Exosomes are nano‐sized vesicles released by a variety of cells. Exosomes function as versatile promoters in the tumorigenesis, metastasis and drug resistance of breast cancer. In this review, we summarize the current knowledge about the functions of exosomes in the diagnosis, tumorigenesis, metastasis, microenvironment, drug resistance and therapy of breast cancer.

Adriamycin and docetaxel are two agents commonly used in treatment of breast cancer, but their efficacy is often limited by the emergence of chemoresistance. Recent studies indicate that exosomes act as vehicles for exchange of genetic cargo between heterogeneous populations of tumor cells, engendering a transmitted drug resistance for cancer development and progression. However, the specific contribution of breast cancer-derived exosomes is poorly understood. Here we reinforced other's report that human breast cancer cell line MCF-7/S could acquire increased survival potential from its resistant variants MCF-7/Adr and MCF-7/Doc. Additionally, exosomes of the latter, A/exo and D/exo, significantly modulated the cell cycle distribution and drug-induced apoptosis with respect to S/exo. Exosomes pre-treated with RNase were unable to regulate cell cycle and apoptosis resistance, suggesting an RNA-dependent manner. Microarray and polymerase chain reaction for the miRNA expression profiles of A/exo, D/exo, and S/exo demonstrated that they loaded selective miRNA patterns. Following A/exo and D/exo transfer to recipient MCF-7/S, the same miRNAs were significantly increased in acquired cells. Target gene prediction and pathway analysis showed the involvement of miR-100, miR-222, and miR-30a in pathways implicated in cancer pathogenesis, membrane vesiculation and therapy failure. Furthermore, D/exo co-culture assays and miRNA mimics transfection experiments indicated that miR-222-rich D/exo could alter target gene expression in MCF-7/S. Our results suggest that drug-resistant breast cancer cells may spread resistance capacity to sensitive ones by releasing exosomes and that such effects could be partly attributed to the intercellular transfer of specific miRNAs.

Apple trees face various challenges during cultivation. Apple leaves, as the key part of the apple tree for photosynthesis, occupy most of the area of the tree. Diseases of the leaves can hinder the healthy growth of trees and cause huge economic losses to fruit growers. The prerequisite for precise control of apple leaf diseases is the timely and accurate detection of different diseases on apple leaves. Traditional methods relying on manual detection have problems such as limited accuracy and slow speed. In this study, both the attention mechanism and the module containing the transformer encoder were innovatively introduced into YOLOV5, resulting in YOLOV5-CBAM-C3TR for apple leaf disease detection. The datasets used in this experiment were uniformly RGB images. To better evaluate the effectiveness of YOLOV5-CBAM-C3TR, the model was compared with different target detection models such as SSD, YOLOV3, YOLOV4, and YOLOV5. The results showed that YOLOV5-CBAM-C3TR achieved mAP@0.5, precision, and recall of 73.4%, 70.9%, and 69.5% for three apple leaf diseases including Alternaria blotch, Grey spot, and Rust. Compared with the original model YOLOV5, the mAP 0.5increased by 8.25% with a small change in the number of parameters. In addition, YOLOV5-CBAM-C3TR can achieve an average accuracy of 92.4% in detecting 208 randomly selected apple leaf disease samples. Notably, YOLOV5-CBAM-C3TR achieved 93.1% and 89.6% accuracy in detecting two very similar diseases including Alternaria Blotch and Grey Spot, respectively. The YOLOV5-CBAM-C3TR model proposed in this paper has been applied to the detection of apple leaf diseases for the first time, and also showed strong recognition ability in identifying similar diseases, which is expected to promote the further development of disease detection technology.

Evolutionarily conserved DDB1‐and CUL4‐associated factor 13 (DCAF13) is a recently discovered substrate receptor for the cullin RING‐finger ubiquitin ligase 4 (CRL4) E3 ubiquitin ligase that regulates cell cycle progression. DCAF13 is overexpressed in many cancers, although its role in breast cancer is currently elusive. In this study we demonstrate that DCAF13 is overexpressed in human breast cancer and that its overexpression closely correlates with poor prognosis, suggesting that DCAF13 may serve as a diagnostic marker and therapeutic target. We knocked down DCAF13 in breast cancer cell lines using CRISPR/Cas9 and found that DCAF13 deletion markedly reduced breast cancer cell proliferation, clone formation, and migration both in vitro and in vivo. In addition, DCAF13 deletion promoted breast cancer cell apoptosis and senescence, and induced cell cycle arrest in the G1/S phase. Genome‐wide RNAseq analysis and western blotting revealed that loss of DCAF13 resulted in both mRNA and protein accumulation of p53 apoptosis effector related to PMP22 (PERP). Knockdown of PERP partially reversed the hampered cell proliferation induced by DCAF13 knockdown. Co‐immunoprecipitation assays revealed that DCAF13 and DNA damage‐binding protein 1 (DDB1) directly interact with PERP. Overexpression of DDB1 significantly increased PERP polyubiquitination, suggesting that CRL4DCAF13 E3 ligase targets PERP for ubiquitination and proteasomal degradation. In conclusion, DCAF13 and the downstream effector PERP occupy key roles in breast cancer proliferation and potentially serve as prognostics and therapeutic targets. DCAF13 is overexpressed in breast cancer and its overexpression closely correlates with the poor prognosis. DCAF13 deletion markedly decreased breast cancer cell proliferation, clone formation, and migration both in vitro and in vivo.DCAF13 promotes breast cancer cell proliferation by inhibiting the expression of PERP.

Conventional wisdom posits that spin-triplet energy transfer (TET) is only operative over short distances because Dexter-type electronic coupling for TET rapidly decreases with increasing donor acceptor separation. While coherent mechanisms such as super-exchange can enhance the magnitude of electronic coupling, they are equally attenuated with distance. Here, we report endothermic charge-transfer-mediated TET as an alternative mechanism featuring shallow distance-dependence and experimentally demonstrated it using a linked nanocrystal-polyacene donor acceptor pair. Donor-acceptor electronic coupling is quantitatively controlled through wavefunction leakage out of the core/shell semiconductor nanocrystals, while the charge/energy transfer driving force is conserved. Attenuation of the TET rate as a function of shell thickness clearly follows the trend of hole probability density on nanocrystal surfaces rather than the product of electron and hole densities, consistent with endothermic hole-transfer-mediated TET. The shallow distance-dependence afforded by this mechanism enables efficient TET across distances well beyond the nominal range of Dexter or super-exchange paradigms. Spin-triplet energy transfer in molecular systems underlies important applications for chemistry and devices. Here, the authors investigate the triplet energy transfer in CdSe quantum dots with varying ZnS shell thicknesses to surface-anchored anthracene molecules and identify a stepwise mechanism mediated by endothermic charge-transfer states.

Anthocyanin accumulation specifically depends on sucrose (Suc) signaling. However, the molecular basis of this process remains unknown. In this study, in vitro pull-down assays identified ETHYLENE-INSENSITIVE3 (EIN3), a component of both sugar signaling or/and metabolism. This protein interacted with YDA, and the physiological relevance of this interaction was confirmed by in planta co-immunoprecipitation, yeast two-hybrid (Y2H) assay, and bimolecular fluorescence complementation. Ethylene insensitive3-like 1 (eil1) ein3 double-mutant seedlings, but not ein3-1 seedlings, showed anthocyanin accumulation. Furthermore, ein3-1 suppressed anthocyanin accumulation in yda-1 plants. Thus, EMB71/YDA-EIN3-EIL1 may form a sugar-mediated gene cascade integral to the regulation of anthocyanin accumulation. Moreover, the EMB71/YDA-EIN3-EIL1 gene cascade module directly targeted the promoter of Transparent Testa 8 (TT8) by direct EIN3 binding. Collectively, our data inferred a molecular model where the signaling cascade of the YDA-EIN3-TT8 appeared to target TT8 via EIN3, thereby modulating Suc signaling–mediated anthocyanin accumulation.

Radiation therapy is recognized as an effective modality in the treatment of lung cancer, but radioresistance resulting from prolonged treatment reduces the chances of recovery. MicroRNAs (miRNAs) play a pivotal role in radiotherapy immunity. In this study, we aimed to investigate the mechanism by which miR‐196a‐5p affects radioresistance in lung cancer. The radioresistant lung cancer cell line A549R26–1 was established by radiation treatment. Cancer‐associated fibroblasts (CAFs) and normal fibroblasts (NFs) were observed by microscopy, and the expression levels of CAF‐specific marker proteins were detected by immunofluorescence. The shape of the exosomes was observed by electron microscopy. A CCK‐8 assay was used to detect cell viability, while clone formation assays were used to detect cell proliferative capacity. Flow cytometry was performed to investigate apoptosis. The binding of miR‐196a‐5p and NFKBIA was predicted and further verified by the dual luciferase reporter experiment. qRT–PCR and western blotting were used to detect gene mRNA and protein levels. We found that exosomes secreted by CAFs could enhance lung cancer cell radioresistance. Moreover, miR‐196a‐5p potentially bound to NFKBIA, promoting malignant phenotypes in radioresistant cells. Furthermore, exosomal miR‐196a‐5p derived from CAFs increased radiotherapy immunity in lung cancer. Exosomal miR‐196a‐5p derived from CAFs enhanced radioresistance in lung cancer cells by downregulating NFKBIA, providing a new potential target for the treatment of lung cancer.

Myeloid-derived suppressor cells (MDSCs) are newly identified immature myeloid cells that are characterized by the ability to suppress immune responses and expand during cancer, infection, and inflammatory diseases. Although MDSCs have attracted a lot of attention in the field of tumor immunology in recent years, little is known about their multiple roles in hematological malignancies as opposed to their roles in solid tumors. This review will help researchers better understand the various characteristics and functions of MDSCs, as well as the potential therapeutic applications of MDSCs in hematological malignancies, including lymphoma, multiple myeloma, leukemia, and hematopoietic stem cell transplantation.

Propionate is one of the most important intermediates of anaerobic fermentation. Its oxidation performed by syntrophic propionate-oxidizing bacteria coupled with hydrogenotrophic methanogens is considered to be a rate-limiting step for methane production. However, the current understanding of SPOB is limited due to the difficulty of pure culture isolation. In the present study, two anaerobic chemostats fed with propionate as the sole carbon source were operated at different dilution rates (0.05 d −1 and 0.15 d −1 ). The propionate- and acetate-oxidizing bacteria in the two methanogenic chemostats were investigated combining DNA-stable isotope probing (DNA-SIP) and 16S rRNA gene high-throughput sequencing. The results of DNA-SIP with 13 C-propionate/acetate suggested that, Smithella , Syntrophobacter , Cryptanaerobacter , and unclassified Rhodospirillaceae may be putative propionate-oxidizing bacteria; unclassified Spirochaetaceae , unclassified Synergistaceae , unclassified Elusimicrobia , Mesotoga , and Gracilibacter may contribute to acetate oxidation; unclassified Syntrophaceae and Syntrophomonas may be butyrate oxidizers. By DNA-SIP, unclassified OTUs with 16S rRNA gene abundance higher than 62% of total Bacteria in the PL chemostat and 38% in the PH chemostat were revealed to be related to the degradation of propionate. These results suggest that a variety of uncultured bacteria contribute to propionate degradation during anaerobic digestion. The functions and metabolic characteristics of these bacteria require further investigation.