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Heart transplantation is an effective method for the treatment of end-stage heart disease. Therefore, this article aimed to establish a stable and effective mouse abdominal heart transplantation model. MiR155 alleviates the acute heart transplantation response by regulating Th1 / Th17 immune cytokines. This paper used the control method of randomly selecting samples to classify 30 healthy mice that met the conditions. First, C57BL / 6 mice were used as recipients, and Balb / c mouse hearts were used as donors to establish mouse hearts as a transplantation acute reaction model. A chronic rejection model of mouse heart transplantation was established by C57BL / 6 mice as recipients and Bm12 mouse hearts as donors. The survival time of the two groups of transplanted hearts was carefully recorded. The results of the study showed that in the heart transplantation acute/chronic rejection model, the average survival time of the donor's heart in the allograft group was (7.5 ± 0.37) / (63.4 ± 4.37) days, which was the same compared with the two groups. Therefore, in-depth analysis of the experimental control results and conclusions from the experimental results of the mice, this study can better respond to the pathological changes of acute/chronic rejection and reach the standard of model establish.

Impact Statement: Nasopharyngeal cancer is one of the most common malignant tumors in the head and neck. Identification of promising miRNA biomarkers might benefit a lot to the detection of nasopharyngeal carcinoma. A three-miRNA signature (has-miR-142-3p, has-miR-29c, and has-miR-30e) was obviously associated with the overall survival of nasopharyngeal carcinoma patients. The model has better clinical independence and has better clinical prediction effect when combined with clinical characteristics. Our results revealed that a three-miRNA signature was a potential novel prognostic biomarker for nasopharyngeal carcinoma.

RNA-binding proteins have been associated with cancer development. The overexpression of a well-known RNA-binding protein, insulin-like growth factor 2 messenger RNA-binding protein 3, has been identified as an indicator of poor prognosis in patients with various types of cancer. Although gastric cancer is a relatively frequent and potentially fatal malignancy, the mechanism by which insulin-like growth factor 2 messenger RNA-binding protein 3 regulates the development of this cancer remains unclear. This study aimed to investigate the role and regulatory mechanism of insulin-like growth factor 2 messenger RNA-binding protein 3 in gastric cancer. An analysis of IGF2BP3 expression patterns reported in 4 public gastric cancer-related microarray data sets from the Gene Expression Omnibus and The Cancer Genome Atlas-Stomach Adenocarcinoma revealed strong expression of this gene in gastric cancer tissues. Insulin-like growth factor 2 messenger RNA-binding protein 3 expression in gastric cancer was further confirmed via quantitative reverse transcription polymerase chain reaction and immunohistochemistry, respectively, in an in-house gastric cancer cohort (n = 30), and the association of insulin-like growth factor 2 messenger RNA-binding protein 3 expression with clinical parameters and prognosis was analyzed. Notably, stronger IGF2BP3 expression significantly correlated with poor prognosis, and significant changes in insulin-like growth factor 2 messenger RNA-binding protein 3 expression were only confirmed in patients with advanced-stage gastric cancer in an independent cohort. The effects of insulin-like growth factor 2 messenger RNA-binding protein 3 on cell proliferation were confirmed through in vitro experiments involving the HGC-27 gastric cancer cell line. MicroR-125a-5p, a candidate microRNA that target on insulin-like growth factor 2 messenger RNA-binding protein 3, decreased in advanced-stage gastric cancer. Upregulation of microR-125a-5p inhibited insulin-like growth factor 2 messenger RNA-binding protein 3, and dual-luciferase report assay indicated that microR-125a-5p inhibited the translation of IGF2BP3 by directly targeting the 3' untranslated region. These results indicate that the microR-125a-5p/insulin-like growth factor 2 messenger RNA-binding protein 3 axis contributes to the oncogenesis of advanced gastric cancer.

Objective: It has been demonstrated that preeclampsia is associated with alterations in placental microRNA expression. Previous reports have shown that hsa-miR-181a-5p is overexpressed in human preeclamptic placenta compared with normotensive placenta. The purpose of this study was to explore whether upregulated hsa-miR-181a-5p expression is involved in the ontogenesis of preeclampsia., Methods: Twenty preeclamptic placentas and 20 normotensive placentas were obtained from nulliparous women by cesarean section. Expression of hsa-miR-181a-5p in placenta tissues and human trophoblast cell lines was analyzed by reverse transcription polymerase chain reaction. The trophoblast cell lines (HTR-8/SVneo and JAR) were transfected with specific oligonucleotides to upregulate miR-181a-5p expression. The effect of miR-181a-5p expression on proliferation, cell cycle, apoptosis, and invasion in HTR-8/SVneo and JAR cells was then investigated., Result: It was demonstrated that hsa-miR-181a-5p expression was upregulated in preeclamptic placentas and that it may trigger antiproliferation and inhibition of cell cycle progression, induce apoptosis, and suppress invasion in HTR-8/SVneo and JAR cells., Conclusion: Anomalously upregulated hsa-miR-181a-5p expression could contribute to trophoblast dysfunction and may be a crucial factor in the pathogenesis of preeclampsia.

Pancreatic cancer is an aggressive malignancy with an extremely poor prognosis. The human ether-a-go-go-related potassium channel (HERG1) is a human rapid delayed rectifier, which is involved in many crucial cellular events. In this article, we find that HERG1 expression is dramatically increased both in pancreatic cancer tissues and cell lines, and that increased HERG1 expression is significantly related to the development of pancreatic cancer. HERG1 silencing in pancreatic cancer-derived cell lines PANC-1 and CFPAC-1 strongly inhibits their malignant capacity in vitro as well as tumorigenicity and metastasis in nude mice. In addition, HERG1 is identified as a direct target of miR-96, which is downregulated in pancreatic cancer tissues and cell lines. Ectopic expression of miR-96 represses the HERG1 expression in pancreatic cancer and significantly inhibits malignant behavior of pancreatic cancer cells in vitro and in vivo. Collectively, our findings suggest that miR-96 acts as a tumor suppressor in pancreatic cancer and may therefore serve as a useful therapeutic target for the development of new anticancer therapy.

MicroRNAs (miRNAs) are known to regulate plant development, but have not been studied in gymnosperm seed tissues. The presence and characteristics of several miRNAs were examined in zygotic embryos (ZEs) and female gametophytes (FGs) of Pinus taeda (loblolly pine). Evidence for miRNAs was obtained using northern analyses and quantitative reverse transcription polymerase chain reaction (qRT-PCR) mediated with poly(A) polymerase. Partial sequences of two miRNAs were verified. Three regions of putative mRNA targets were analyzed by qRT-PCR to monitor the occurrence of stage-dependent miRNA-mediated cleavage. Five miRNAs were identified in ZEs and FGs along with partial sequences of Pta-miR166 and Pta-miR167. Both miRNAs showed differing degrees of tissue-specific and stage-specific modulation. Analysis of HB15L mRNA (a potential Pta-miR166 target) suggested miRNA-guided cleavage in ZEs and FGs. Analysis of ARF8L mRNA (a potential Pta-miR167 target) implied cleavage in ZEs but not in FGs. Argonaute9-like mRNA (ptAGO9L) showed stage-specific modulation of expression in ZEs that appeared to be inverted in the corresponding FGs. MicroRNAs and argonaute genes varied spatiotemporally during seed development. The peak levels of Pta-miR166 in FGs and ptAGO9L in embryos occurred at stage 9.1, a critical transition point during embryo development and a point where somatic embryo maturation often stops. MicroRNAs identified in FG tissue may play a role in embryogenesis.