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Purpose: The aim of the present study was to test the hypothesis that recovery sleep could counteract the detrimental effects of sleep deprivation (SD) on male rats’ fertility. Materials and Methods: Twenty-two rats were housed in groups of six per cage with unrestricted access to food and water in a room. The modified multiple platform method was used to induce SD in rats over a 96-hour period. We examined the effect of SD on semen quality, reproductive hormones, and testicular histology in adult male rats. Then, we investigated the effect of 7 days recovery sleep on impaired reproductive function induced by SD. Results: After the acclimation period, 22 rats were randomly separated into three experimental groups (SD, recovery sleep, and the control groups). Ninety-six hours of SD resulted in a significant decrease in sperm motility (24.33±10.93 vs . 48.20±8.55, p

Abstract Circular RNA HIPK3 (circHIPK3) mediates the progression of multiple cancers, including bladder cancer, by regulating cell migration, autophagy and epithelial mesenchymal transition. However, the mechanism by which circHIPK3 regulates autophagy in bladder cancer cells remains unclear. Autophagy is a common self-protection mechanism in eukaryotic cells and is essential for cell survival and death regulation. However, it is unclear whether circHIPK3 affects the level of autophagy in bladder cancer through binding proteins, and the potential regulatory mechanism is unknown. Here, we found that circHIPK3 levels were significantly lower and autophagy-related proteins were significantly upregulated in bladder cancer cells and tissues compared to normal controls. CircHIPK3 downregulation promoted bladder cancer cell proliferation, while circHIPK3 overexpression inhibited proliferation. CircHIPK3 overexpression significantly suppressed autophagy in bladder cancer cells. Overexpression of circHIPK3 did not affect VCP protein expression but inhibited the VCP/Beclin 1 interaction. VCP also stabilized Beclin 1 and promoted autophagy in bladder cancer cells by downregulating ataxin-3. Thus, circHIPK3 may play an important role in bladder cancer by inhibiting VCP-mediated autophagy.

PurposeThere is evidence that the Crystallin Alpha B (CRYAB) gene is involved in the regulation of the tumor microenvironment and influences tumor prognosis in some cancers. However, the role of CRYAB gene in prognosis and immunology in pan-cancer is still unclear.MethodsIn this study, we analyzed the transcriptional profiles and survival data of cancer patients from The Cancer Genome Atlas (TCGA) database. CRYAB gene and its relationships with pan-cancer were analyzed using R packages, TIMER2.0, GEPIA2, Sangerbox, UALCAN, cBioPortal, ESTIMATE algorithm, and STRING. Besides, real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was utilized to detect CRYAB expression in KIRC and a human KIRC cell line (Caki-1).ResultsWe found that CRYAB expression was different in tumors and adjacent tumors in human cancers, affecting patients’ prognosis in 15 cancer types. Additionally, CRYAB expression significantly correlated with tumor microenvironment (TME), immune checkpoints (ICP), tumor mutational burden (TMB), and microsatellite instability (MSI) in human cancers. Besides, CRYAB expression was positively associated with the immune infiltration of cancer-associated fibroblasts (CAFs) and endothelial cells in most human cancers. Based on enrichment analysis, the most prevalent CRYAB gene mechanism in malignant tumors may be through anti-apoptotic activity. Moreover, some FDA-approved drugs were found to be associated with CRYAB and might be potential cancer therapeutic candidates.ConclusionsCRYAB is a crucial component of the TME and influences immune cell infiltration, making it a promising biomarker to assess immune infiltration and prognosis in many malignancies.

Increasing evidence suggests that microRNAs (miRNAs) play critical roles in bladder tumorigenesis and development by combining with the 3’ untranslated regions (3’-UTRs) of the corresponding mRNAs to negatively regulate gene expression. The role of miR-182-5p in bladder cancer (BC) remains unclear. Therefore, this study aimed to clarify the functional role of miR-182-5p in BC. We predicted candidate mRNAs for miR-182-5p via three databases (TarBase, ENCORI, and miRDB). Dual-luciferase reporter assays and target prediction confirmed FOXF2 as a potential target of miR-182-5p. Quantitative RT-PCR (qRT-PCR) showed that endogenous miR-182-5p expression was significantly upregulated in BC cell lines and clinical samples of BC patients. IHC, western blotting, and qRT-PCR assays indicated that FOXF2 expression was concurrently downregulated in BC tissues and BC cell lines. Gain- and loss-of-function studies showed that the overexpression of miR-182-5p enhanced the proliferation and migration of BC cells, while the downregulation of miR-182-5p showed the opposite results. The effects induced by miR-182-5p were attenuated with the restoration of FOXF2 expression. In BC cells, the upregulation of miR-182-5p not only decreased FOXF2 expression but also markedly increased Sonic hedgehog (SHH) pathway levels. These findings suggested that FOXF2 directly binds to miR-182-5p and that miR-182-5p acts as a tumor promoter in BC genesis and metastasis by targeting FOXF2. In addition, miR-182-5p plays a pro-cancer role by downregulating FOXF2 and activating the SHH pathway. [ABSTRACT FROM AUTHOR]