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Snail2 has an important role in the epithelial-mesenchymal transition (EMT) and tumor metastasis. Here, we report that Snail2 is highly expressed during TGF-β induced EMT in HL-7702 cells. Additionally, overexpression of Snail2 successfully promotes the migration and invasion of these cells, both in vitro and in a mouse model. Furthermore, our results show that HDAC1 and HDAC3 could suppress the Snail2 gene promoter. Moreover, we find that the acetylation of H3K4 and H3K56 are significantly reduced during the EMT process of liver HL-7702 cells. Thus, our results indicate that HDAC1 and HDAC3 epigenetically suppress the expression of Snail2 during the EMT of liver cells, revealing an opposing function of HDACs during the migration of malignant tumors.Adenosine-to-inosine (A-to-I) editing and N6-methyladenosine (m6A) are two of the most abundant RNA modifications. Here, we examined the characteristics of the RNA editing and transcriptome-wide m6A modification profile in the gonads of the olive flounder, Paralichthys olivaceus, an important maricultured fish in Asia. The gonadal differentiation and development of the flounder are controlled by genetic as well as environmental factors, and the epigenetic mechanism may play an important role. In total, 742 RNA editing events were identified, 459 of which caused A to I conversion. Most A-to-I sites were located in 3’UTRs, while 61 were detected in coding regions (CDs). The number of editing sites in the testis was higher than that in the ovary. Transcriptome-wide analyses showed that more than one-half of the transcribed genes presented an m6A modification in the flounder gonads, and approximately 60% of the differentially expressed genes (DEGs) between the testis and ovary appeared to be negatively correlated with m6A methylation enrichment. Further analyses revealed that the mRNA expression of some sex-related genes (e.g., dmrt1 and amh) in the gonads may be regulated by changes in mRNA m6A enrichment. Functional enrichment analysis indicated that the RNA editing and m6A modifications were enriched in several canonical pathways (e.g., Wnt and MAPK signaling pathways) in fish gonads and in some pathways whose roles have not been investigated in relation to fish sex differentiation and gonadal development (e.g., PPAR and RNA degradation pathways). There were 125 genes that were modified by both A-to-I editing and m6A, but the two types of modifications mostly occurred at different sites. Our results suggested that the presence of sex-specific RNA modifications may be involved in the regulation of gonadal development and gametogenesis.Up to 30% of women experience early miscarriage due to impaired decidualization. For implantation to occur, the uterine endometrial stromal fibroblast-like cells must differentiate into decidual cells, but the genes required for decidualization have not been fully defined. Here, we show that Malignant Brain Tumor Domain-containing Protein 1 (MBTD1), a member of the polycomb group protein family, is critical for human endometrial stromal cell (HESC) decidualization. MBTD1 predominantly localized to HESCs during the secretory phase and the levels were significantly elevated during in vitro decidualization of both immortalized and primary HESCs. Importantly, siRNA-mediated MBTD1 knockdown significantly impaired in vitro decidualization of both immortalized and primary HESCs, as evidenced by reduced expression of the decidualization markers PRL and IGFBP1. Further, knockdown of MBTD1 reduced cell proliferation and resulted in G2/M cell cycle arrest in decidualizing HESCs. I-BET151 Although progesterone signaling is required for decidualization, MBTD1 expression was not affected by progesterone signaling; however, MBTD1 knockdown significantly reduced expression of the progesterone target genes WNT4, FOXOA1, and GREB1. Collectively, our data suggest that MBTD1 contributes to in vitro decidualization of HESCs by sustaining progesterone signaling. This work could have implications for designing diagnostic and therapeutic tools for recurrent pregnancy loss.Endogenous repair after chronic compressive spinal cord injury (CCSCI) is of great clinical interest. Ischemia-hypoxia-induced angiogenesis has been proposed to play an important role during this repair process. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathophysiological processes of various diseases. Here, we identified a lncRNA (Xist; X-inactive specific transcript) with upregulated expression in cervical spine lesions during endogenous neurological repair in CCSCI rats. Therapeutically, the introduction of Xist to rats increased neurological function in vivo as assayed using the Basso, Beattie, and Bresnahan (BBB) score and inclined plane test (IPT). We found that the introduction of Xist enhanced endogenous neurological repair by promoting angiogenesis and microvessel density after CCSCI, while depletion of Xist inhibited angiogenesis and cell sprouting and migration. Mechanistically, Xist promoted angiogenesis by sponging miR-32-5p and modulating Notch-1 expression both in vitro and in vivo. These findings suggest a role of the Xist/miR-32-5p/Notch-1 axis in endogenous repair and provide a potential molecular target for the treatment of ischemia-related central nervous system (CNS) diseases.Translationally controlled tumor protein (TCTP) is a multifunctional protein implicated in various types of cellular processes involving growth and development of an organism. Here, we identified tctp gene in Dictyostelium discoideum and unraveled its function. The sequence analysis of D. discoideum TCTP (DdTCTP) showed its conservation among eukaryotes. Transcript of DdTCTP was highly expressed at the initial time points of development and protein is localized both in the cytoplasm and nucleus. Disruption of tctp was achieved by BSR cassette using double homologous recombination method. Abrogation of tctp resulted in reduced cell proliferation but increased cell size. Additionally, development was delayed by 4 h wherein small-sized aggregates and fruiting bodies were produced by tctp- cells while larger aggregates and fruiting bodies were produced by tctp OE cells concordant with the fact that TCTP regulates prestalk/prespore ratio and cell-type differentiation. tctp- cells produced round spores with reduced viability and stalk cells are arranged in septate pattern as compared to polyhedral manner of wild type.