Over recent years, online purchase platforms of fruits are increasingly emerged to advance the e-commerce development and improve quality of human life. Unfortunately, we empirically observed that a lot of enterprises selling fruits online have suffered from bankruptcy due to a lot of complicated factors, such as inefficient logistics, low acceptance of online platforms, and financial risks. One of the root causes responsible for such an unanticipated phenomenon is related to the purchase intention, which motivates us to investigate what are the dominant factors affecting the online purchase intention of fruits. The results can be of great significance to the development of fruit e-commerce enterprises in online marketing. Based on the technology acceptance model (TAM) and perceived risk theory (PRT), this research developed an integrated theoretical model to explore the influential factors underlying consumers' intention to purchase fruits online. A web-based survey of 344 consumers with ages below 30 was used to test the hypotheses in our theoretical model. Through sample collection with questionnaires, a structural equation model is developed to compute the coupling relationship between influential factors and purchase intention. The results reveal that fruit quality and price are dominantly affecting the willingness of consumers to purchase fruit. Surprisingly, we found that e-commerce platforms, information quality, and perceived risk are less significant. Finally, some specific suggestions are recommended for fruit e-commerce enterprises in devising effective marketing strategies.

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Salt-inducible kinase (SIK), which belongs to the sucrose non-fermenting 1/AMP-activated protein kinase family, was first discovered in the adrenal cortex of a rat on a high-salt diet. As an isoform of the SIK family, SIK2 modulates various biological functions and acts as a signal transmitter in various pathways. Compared with that in adjacent normal tissues, the expression of SIK2 is significantly higher in multiple types of tumors, which indicates its pivotal effect in oncogenesis. Studies on SIK2 have recently underlined its role in several signaling pathways, including the PI3K-Akt-mTOR pathway, the Hippo-YAP pathway, the LKB1-HDAC axis, and the cAMP-PKA axis. Moreover, a few small-molecule SIK2 inhibitors have been found to be able to rescue the oncogenicity of SIK2 during tumor development and reverse its abnormal activation of downstream pathways. In this mini-review, we discuss the results of in vivo and in vitro studies regarding the SIK2 mechanism in different signaling pathways, particularly their regulation of cancer cells. This work may provide new ideas for targeting SIK2 as a novel therapeutic strategy in tumor therapy.

Background Radiotherapy resistance is a major obstacle in the treatment of oesophageal squamous cell carcinoma (OSCC). Hypoxia is a critical cause of radioresistance. However, the communication between hypoxic cells and aerobic cells via exosomes during the transfer of radiation resistance remains unclear. Methods Exo-miR-340-5p levels were analysed by RNA-seq and qRT-PCR. We co-cultured OSCC cells with isolated normoxic and hypoxic exosomes to study their impact on radiosensitivity. We used a specific exo-miR-340-5p mimic and knock-down retrovirus to explore the role of this miRNA in the transfer of radioresistance from hypoxic to normoxic cells. Dual-luciferase reporter and RIP assays were used to verify KLF10 as a putative target of miR-340-5p. Several in vitro assays were conducted and xenograft models were established to investigate the effect of exo-miR-340-5p on OSCC radiosensitivity. The plasma exo-miR-340-5p levels in OSCC patients were analysed to study the clinical value of this parameter. Results Hypoxic exosomes alleviated radiation-induced apoptosis and accelerated DNA damage repair. miR-340-5p was highly expressed in hypoxic exosomes and was transferred into normoxic cells, where it induced radioresistance. Overexpression of miR-340-5p in normoxic OSCC cells mimicked the radioresistance of cells co-cultured with hypoxic exosomes. Knockdown of miR-340-5p in hypoxic exosomes reversed the radioresistance effect, indicating that exo-miR-340-5p is critical for hypoxic EV-transferred radioresistance. KLF10 was identified as the direct target of miR-340-5p. Moreover, metformin was found to increase the expression of KLF10 and enhance the radiosensitivity of OSCC. Higher levels of miR-340-5p in the plasma exosomes from OSCC patients are related to a poorer radiotherapy response and prognosis. Conclusions Hypoxic tumour cell-derived exosomal miR-340-5p confers radioresistance in OSCC by targeting KLF10/UVRAG, suggesting that miR-340-5p could be a potential biomarker and therapeutic target for the enhancement of radiosensitivity in OSCC. Metformin can increase KLF10 expression, which ameliorates the radioresistance induced by exo-miR-340-5p transfer. Therefore, metformin could be further investigated as a therapeutic option for the treatment of OSCC.

Background Extracellular vesicles (EVs) are endogenous membrane vesicles with a diameter of 30–200 nm. It has been reported that hypoxic cancer cells can release numerous EVs to mediate multiple regional and systemic effects in the tumor microenvironment. Methods In this study, we used ultracentrifugation to extract EVs secreted by TE‐13, an esophageal squamous carcinoma (ESCC) cell line during normoxia and hypoxia and performed high‐throughput sequencing to detect exosomal miRNAs. Gene ontology (GO) and KEGG pathway analyses were used to reveal pathways potentially regulated by the miRNAs. Results A total of 10 810 miRNAs were detected; 50 were significantly upregulated and 34 were significantly downregulated under hypoxic environment. GO analysis identified enrichment of protein binding, regulation of transcription (DNA‐templated), and membrane as molecular function, biological process, and cellular component, respectively. KEGG pathway analysis revealed cancer‐associated pathways, phospholipase D signaling pathway, autophagy, focal adhesion and AGE‐RAGE signaling as the key pathways. Further verification experiment from qRT‐PCR indicated that miR‐128‐3p, miR‐140‐3p, miR‐340‐5p, miR‐452‐5p, miR‐769‐5p and miR‐1304‐p5 were significantly upregulated in EVs from hypoxia TE‐13 cells while miR‐340‐5p was significantly upregulated in two other ESCC cells, ECA109 and TE‐1. Conclusion This study, for the first time reveals changes in the expression of exosomal miRNAs in hypoxic ESCC cells and these findings will act as a resource to study the hypoxic tumor microenvironment and ESCC EVs.

MicroRNAs (miRNAs) are non-coding small RNA molecules that regulate gene expression at the post-transcriptional/translational level. They act a considerable role not only in the normal progress of development but also in aberrant human diseases, including malignancy. With accumulating proofs of miR-105, the complex role of miR-105 during cancer initiation and progression is gradually emerging. miR-105 acts as a tumor suppressor by inhibiting tumor growth and metastasis or as an oncogene by promoting tumor initiation and invasion, depending on particular tumor contexts and base-pairing genes. In this review, we emphasize the characteristics of miR-105 in cancer to elucidate various deadly tumors and discuss transcriptional regulations that may explain fluctuations in miR-105 expression. This review may provide new ideas for applying miR-105 as a diagnostic and prognostic biomarker.

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Grain shape is controlled by quantitative trait loci (QTLs) in rice (Oryza sativa L.). A rice mutant (JF178) with long and large grains has been used in a breeding program for over a decade, but its genetic basis has been unclear. Here, a semi-dominant QTL, designated Large Grain Size 1 (LGS1), was cloned and the potential molecular mechanism of LGS1 function was studied. Near-isogenic lines (NILs) and a map-based approach were employed to clone the LGS1 locus. LGS1 encodes the OsGRF4 transcription factor and contains a 2 bp missense mutation in the coding region that coincides with the putative pairing site of miRNA396. The LGS1 transcript levels in the mutant line were found to be higher than the lgs1 transcript levels in the control plants, suggesting that the mutation might disrupt the pairing of the LGS1 mRNA with miR396. In addition to producing larger grains, LGS1 also enhanced cold tolerance at the seedling stage and increased the survival rate of seedlings after cold stress treatment. These findings indicate that the mutation in LGS1 appears to disturb the GRF4–miR396 stress response network and results in the development of enlarged grains and enhancement of cold tolerance in rice.