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Chromosomal ploidy manipulation is one of the means to create excellent germplasm . Triploid fish could provide an ideal sterile model for searching of a underlying mechanism of abnormality in meiosis. The complete understanding of the coding and noncoding RNAs regulating sterility caused by meiosis abnormality is still not well understood. By high-throughput sequencing, we compared the expression profiles of gonadal mRNA, long non-coding RNA (lncRNA), and microRNA (miRNA) at three different developmental stages between the diploid (XX) and triploid (XXX) female rainbow trout . These stages were gonads before differentiation (65 days post fertilisation, dpf), at the beginning of morphological differences (180 dpf) and showing clear difference between diploids and triploids (600 dpf), respectively. A majority of differentially expressed (DE) RNAs were identified, and 22 DE mRNAs related to oocyte meiosis and homologous recombination were characterized. The predicted miRNA-mRNA/lncRNA networks of 3 developmental stages were constructed based on the target pairs of DE lncRNA-miRNA and DE mRNA-miRNA. According to the networks, meiosis-related gene of ccne1 was targeted by dre-miR-15a-5p_R + 1, and 6 targeted DE lncRNAs were identified. Also, qRT-PCR was performed to validate the credibility of the network. Overall, this study explored the potential interplay between coding and noncoding RNAs during the gonadal development of polyploid fish. The mRNA, lncRNA and miRNA screened in this study may be helpful to identify the functional elements regulating fertility of rainbow trout, which may provide reference for character improvement in aquaculture.

Wenwen Wei,1,* Baosheng Huo,2,* Xiulan Shi1 1Department of Respiratory Medicine, The Second People’s Hospital of Dongying, Guangrao City, Shandong Province 257335, People’s Republic of China; 2Department of Thoracic Surgery, The Second People’s Hospital of Dongying, Guangrao City, Shandong Province 257335, People’s Republic of China *These authors contributed equally to this work Background: Methyltransferase like 3 (METTL3) is an RNA methyltransferase implicated in mRNA biogenesis, decay, and translation control through N6-methyladenosine (m6A) modification.Methods: To find new treatment strategies for lung cancer and to elucidate the mechanism underlying the phenomenon, we treated the human lung cancer cell lines A549 and H1299 to investigate the effect of METTL3 on lung cancer. Results: We observed that knockdown of METTL3 inhibited the survival and proliferation of A549 and H1299 cells. The migration and proliferation of both cell lines were significantly decreased, and the apoptosis was induced in comparison with control cells. These results were further confirmed by the transfection of miRNA of METTL3 increased the Bax/Bcl-2 ratio in A549 and H1299 cells, which is a sign that mitochondrial apoptotic pathway was triggered. The PI3K/Akt pathway is implicated in cell growth and survival and we also observed that knockdown of METTL3 changed the expression and phosphorylation of proteins of PI3K signaling pathway members. Further, our results demonstrated that miR-600 inhibited the expression of METTL3 and reversed the positive effect of METTL3 on NSCLC progression, indicating an miR-600/METTL3 pathway in NSCLC. Conclusion: These data suggested that miR-600 inhibited lung cancer via down-regulating METTL3 expression, and knockdown of METTL3 might be used as a novel strategy for lung cancer therapy. Keywords: METTL3, miRNA, lung cancer, A549, H1299, apoptosis, PI3K pathway