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Spermatogenesis is a highly orchestrated dynamic developmental process, during which piRNAs play an indispensable role. Our previous studies have confirmed that the levels of piR‐1207 and piR‐2107 were significantly decreased in spermatozoa and seminal plasma of patients with asthenozoospermia, compared with the fertile controls. In order to explore the function of piR‐1207 and piR‐2107 in human spermatogenesis and their potential regulatory downstream genes, we examined the transcriptomic landscape in mouse spermatocyte cell line GC‐2spd(ts) transfected with anti‐piR‐1207 and anti‐piR‐2107 by RNA sequencing. The result showed that 86 and 75 differential expression genes (DEGs) in anti‐piR‐1207 and anti‐piR‐2107 group, respectively. Among the DEGs, three genes including Pbp2, Pde3a and Cage1 were identified as potential key genes playing important roles in mediating sperm motility and morphology in anti‐piR‐1207 or anti‐piR‐2107 transfected transcriptomic response. Next, the expression levels of Pbp2, Pde3a and Cage1 were confirmed by qRT‐PCR. These results showed that Pbp2, Pde3a and Cage1 may serve as the potential regulatory genes of piR‐1207 or piR‐2107. In summary, piR‐1207 and piR‐2107 might have an implication in modulating the process of spermatogenesis through regulating the expression of potential genes. [ABSTRACT FROM AUTHOR]

Lung cancer has high mortality and incidence rates in which non‐small cell lung cancer (NSCLC) is the primary type of lung cancer that accounts for about 80%–85% of total patients. It has been demonstrated that microRNAs (miRNAs) are critical in the incidence and progression of tumors, while the role and inner mechanism of miR‐200a‐3p, one type of essential miRNAs, in NSCLC have yet to be revealed. Herein, we investigated the in vitro and vivo pro‐/antiproliferative influence of miR‐200a‐3p on NSCLC cells and utilized bioinformatic programs to further predict the SOX17 gene as miR‐200a‐3p's potential target. A double luciferase reporter gene experiment was performed to confirm that miR‐200a‐3p interacts with the SOX17 3ʹ‐UTR region specifically. On the basis of the results of Western blot and quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR), miR‐200a‐3p impacted the posttranscriptional levels of SOX17 rather than influencing its mRNA expression. In the end, we found that overexpressed SOX17 can reverse miR‐200a‐3p's impact on NSCLC cell proliferation and metastasis. Therefore, this study demonstrated that miR‐200a‐3p influences NSCLC cell proliferation and metastasis by modulating the levels of SOX17. [ABSTRACT FROM AUTHOR]

Regeneration is a unique defense mechanism of liver tissue in response to functional cell loss induced by toxic chemicals or surgical resection. In this study, we found that Islet‐cell autoantigen 69 (Ica69) accelerates liver regeneration in mice. Following 70% partial hepatectomy, both Ica69 mRNA and protein are significantly upregulated in mouse hepatocytes at the early stage of liver regeneration. Compared with the wild‐type mice, Ica69‐deficient mice have more severe liver injury, delayed liver regeneration, and high surgical accidental mortality following hepatectomy. Mechanistically, Ica69 interacts with Pick1 protein to regulate Tgfbr1 protein expression and Tgfβ‐induced Smad2 phosphorylation. Our findings suggest that Ica69 in liver tissue is a new potential target for promoting liver regeneration. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is a global health problem and one of the most common malignant tumors. Recent studies have shown that noncoding RNAs (ncRNAs) contribute to the pathogenesis of hepatocellular carcinoma (HCC). These RNAs may be involved in a variety of pathological processes such as cell proliferation, apoptosis, angiogenesis, invasion, and metastasis. In addition, abnormal expression of ncRNAs in HCC may provide potential prognostic or diagnostic biomarkers. This review provides an overview of the role and potential applications of ncRNAs, miRNAs, lncRNAs, circRNAs, and snoRNAs in liver cancer. [ABSTRACT FROM AUTHOR]