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  • br Conclusion Blueberry is becoming a


    Conclusion Blueberry is becoming a worldwide crop with the fastest rising consumer demand trends for its health benefits. However, the berry size is one of the key parameters for determining fruit quality and consumers’ preferences (Milic et al., 2018). Understanding the physiological and molecular mechanisms of regulating blueberry WY-14643 fruit size would be promoted for breeding and cultivation. In this study, we found that V. corymbosum flower buds had lower contribution to mature fruit mass, whereas ovary wall was the key tissue for fruit growth, and approximately 70% of pericarp cell layers were formed before anthesis. In addition, 12 V. corymbosum cell-cycle related genes were isolated firstly in this study, and its sequences were relatively conserved. The expression pattern analysis demonstrated that most WY-14643 and CDK genes displayed regular change during the blueberry flower bud enlargement and fruit growth. However, it seemed that there was no correlation between fruit size and Vccyclins and VcCDKs expression levels, indicated that although the cell-cycle related proteins could affect fruit cell production and cell volume, but were not the core factors for regulating fruit size and mass, and relevant mechanisms need to further study.
    Acknowledgements This work was supported by the major program for science and technology of Zhejiang province (grant numbers 2018C02007 and 2016C02052-9), the project of science and technology department of Zhejiang province (grant numbers 2016C32010), and the key project for science and technology program of Jinhua (2016-2-002).
    Introduction Hepatocellular carcinoma (HCC) is the fifth most common malignant tumors and the third cause of cancer-related death worldwide [1]. An estimated report of cancer statistics in China deduces that about 466,100 Chinese are newly diagnosed with HCC, and approximately 422,100 Chinese die from HCC in 2015 year [2]. Although the diagnostic and therapeutic strategies make significant progress in the clinical practice of HCC, a 1-year survival rate is less than 50% [3], which may be attributed to the complicated pathogenic mechanism of HCC. Therefore, it is imperative to further explore the molecular mechanism underlying the hepatic tumorigenesis, which may reveal the new therapeutic targets for improving the survival prognosis of HCC patients. Cyclin-dependent kinase 8 (CDK8) is a ubiquitously expressed transcription-regulating serine/threonine kinases and is belong to CDK family [4]. Recent study reveals that CDK8 plays a positive role in gene-specific transcription by the phosphorylation of transcription factors or the association with the Mediator complex [4]. CDK8-modulated signaling pathways, such as Wnt/β-catenin, estrogen receptor-responsive genes and drosophila mothers against decapentaplegic transcriptional signaling, have been implicated in regulating oncogenesis in breast cancer, pancreatic cancer and colorectal cancer [[4], [5], [6], [7], [8]]. Overexpression of CDK8 is presented in melanoma, breast cancer and prostate cancer [6,9,10]. The suppression of CDK8 expression by small interfering RNA or short hairpin leads to inhibit proliferation in colon cancer, prostate cancer and breast cancer cells [6,8,10]. In addition, CDK8-mediated phosphorylation restrains natural killer (NK) cells cytotoxicity and tumor surveillance, while specific CDK8 deletion in NK cells enhances antitumor responses [11,12]. These promising preclinical data suggest that specific inhibition of CDK8 had the ability to neutralize its oncogenic activity. MicroRNAs (miRNAs) have emerged as a novel class of noncoding RNAs and are characterized by short, noncoding and single-stranded RNAs of ˜22 nucleotides [13,14]. In mammal, more than one-third of genes can be silenced by miRNAs by post-transcriptionally regulatory mechanism via binding with the 3′-untranslated region (3′-UTR) of target genes to repress transcription or translation [13,14]. Numerous studies indicate that miRNAs participate in a variety of biological processes, including carcinogenesis [15]. So far, numerous miRNAs are determined to regulate the progression of HCC, including miR-148-3p/152-3p family members [16]. For example, a decrease in miR-152 expression levels is observed in human HCC tissues [17]. Down-regulation of miR-152 is frequently reported in HBV-related HCC and induces aberrant DNA methylation facilitating the process of HCC [18]. Low level of circulating miR-152 is detected in serum of HCC patients with hepatitis C virus infection as compared to the patients with hepatitis C virus infection alone [19]. These results support a tumor-suppressive role of miR-152 in the progression of HCC. However, the roles of miR-152-3p in hepatic carcinogenesis via targeting CDK8 are still unclear.