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, 2014; Ariyoshi et al., 2017; Shiozaki et al., 2017, 2018a; Kobayashi et al., 2018; Yamazato et al., 2018; Konishi et al., 2019; Kudou et al., 2019; Katsurahara et al., 2020, 2021; Matsumoto et al., 2021; Mitsuda et al., 2021). We have also previously demonstrated the clinicopathological and prognostic significance of their expression in ESCC patients, and shown that their pharmacological blockage and gene silencing had an impact on carcinogenesis, indicating their potential as targets for the treatment of UGI cancers. A more detailed understanding of the molecular regulatory mechanisms underlying cell death and survival of UGI cancers may result in the application of cellular physiological methods as novel therapeutic approaches.Chronic hepatitis B virus (HBV) infection is a risk factor for liver cirrhosis (LC) and hepatocellular carcinoma (HCC), however, little is known about the mechanisms involved in the progression of HBV-related diseases. It has been well acknowledged that host immune response was closely related to the clinical outcomes of patients with HBV infection. As the factors closely related to the immunomodulatory process, cytokines are crucial in the cell-cell communication and the host responses to HBV infection. Recently, a newly discovered cytokine, designated as interleukin-35 (IL-35), has been proved to be essential for the progression of chronic HBV infection, the development of cirrhosis, the transformation of cirrhosis to HCC, and the metastasis of HCC. Specifically, it showed various biological activities such as inhibiting the HBV-specific cytotoxic T lymphocyte (CTL) proliferation and cytotoxicity, deactivating the immature effector T-cells (Teffs), as well as delaying the proliferation of dendritic cells. It regulated the immune responses by acting as a "brake" on the activation of Teffs, which subsequently played important roles in the pathogenesis of various inflammatory diseases and malignancies. In this review, we focused on the most recent data on the relationship between IL-35 and chronic HBV infection, LC and HCC.Satellite cells (SCs) are tissue-specific stem cells responsible for adult skeletal muscle regeneration and maintenance. SCs function is critically dependent on two families of transcription factors the paired box (Pax) involved in specification and maintenance and the Muscle Regulatory Factors (MRFs), which orchestrate myogenic commitment and differentiation. In turn, signaling events triggered by extrinsic and intrinsic stimuli control their function via post-translational modifications, including ubiquitination and phosphorylation. In this context, the Abelson non-receptor tyrosine kinase (c-Abl) mediates the activation of the p38 α/β MAPK pathway, promoting myogenesis. c-Abl also regulates the activity of the transcription factor MyoD during DNA-damage stress response, pausing differentiation. However, it is not clear if c-Abl modulates other key transcription factors controlling SC function. This work aims to determine the role of c-Abl in SCs myogenic capacity via loss of function approaches in vitro and in vivo. Here we show that c-Abl inhibition or deletion results in a down-regulation of Pax7 mRNA and protein levels, accompanied by decreased Pax7 transcriptional activity, without a significant effect on MRF expression. Additionally, we provide data indicating that Pax7 is directly phosphorylated by c-Abl. Finally, SC-specific c-Abl ablation impairs muscle regeneration upon acute injury. Our results indicate that c-Abl regulates myogenic progression in activated SCs by controlling Pax7 function and expression.Urothelial bladder cancer (UBC) is the most common malignant tumor of the urinary system. GsMTx4 Most patients do not benefit from treatment with immune checkpoint inhibitors, which are closely associated with immune profiling in the context of UBC. Therefore, we aimed to characterize the immune profile of UBC to identify different immune subtypes that may influence therapy choice. We identified four subtypes of UBC based on immune profiling including immune ignorant, cold tumor, immune inactive, and hot tumor. After excluding the cold tumor subtype because of its unique pathology distinct from the other types, a high correlation between patient survival and immune characteristics was observed. Most immune cell types had highly infiltrated the hot tumor subtype compared to other subtypes. Interestingly, although immune cells infiltrated the tumor microenvironment, they exhibited an exhaustion phenotype. CCL4 may be the key molecule functioning in immune cell infiltration in the hot tumor subtype. Moreover, neutrophils may function as an important suppressor in the tumor microenvironment of the immune ignorant and immune inactive subtypes. Furthermore, different tumor-intrinsic signaling pathways were involved in immune cell infiltration and exclusion in these four different subtypes. Immune profiling could serve as a prognostic biomarker for UBC, and has potential to guide treatment decisions in UBC. Targeting tumor-intrinsic signaling pathways may be a promising strategy to treat UBC.Lubrication disorder is a common health issue that manifests as insufficient sexual arousal at the beginning of sex. It often causes physical and psychological distress. However, there are few studies on lubrication disorder, and the complexity of circular RNA (circRNA) and the related competing endogenous RNA (ceRNA) network in lubrication disorder is still poorly known. Therefore, this study aims to build a regulatory circRNA-micro (mi)RNA-mRNA network and explore potential molecular markers of lubrication disorder. In the study, 12 subjects were recruited, including 6 in the lubrication disorder group and 6 in the normal control group. RNA sequencing was exploited to identify the expression profiles of circRNA, miRNA and mRNA between two groups, and then to construct the circRNA-miRNA-mRNA networks. The enrichment analyses of the differentially expressed (DE)-mRNAs were examined via Gene Set Enrichment Analysis (GSEA). Furthermore, the expression level and interactions among circRNA, miRNA, and mRNA were validated using real-time quantitative polymerase chain reaction (RT-qPCR) and dual-luciferase reporter assays.