Spermatogonial stem cells (SSCs), a unique population of male germ cells with self‐renewal ability, are the foundation for maintenance of spermatogenesis throughout the life of the male. Although many regulatory molecules essential for SSC self‐renewal have been identified, the fundamental mechanism underlying how SSCs acquire and maintain their self‐renewal activity remains largely to be elucidated. In recent years, many types of noncoding RNAs (ncRNAs) have been suggested to regulate the SSC self‐renewal through multiple ways, indicating ncRNAs play crucial roles in SSC self‐renewal. In this paper, we mainly focus on four types of ncRNAs including microRNA, long ncRNA, piwi‐interacting RNA, as well as circular RNAs, and reviewed their potential roles in SSC self‐renewal that discovered recently to help us gain a better understanding of molecular mechanisms by which ncRNAs perform their function in regulating SSC self‐renewal.

DHX37, a member of the DEAD/H-box RNA helicase family, has been implicated in various diseases, including tumors. However, the biological characteristics and prognostic significance of DHX37 in HCC remain unclear. In this study, we use R software 3.6.3 and multiple bioinformatics analysis tools, such as GDSC, HPA, STRING, TISCH, and TIMER2, to analyze the characterization and function of DHX37 in HCC. In addition, Western blot (WB) and immunohistochemistry (IHC) based on clinical samples validated some of the findings. DHX37 was more highly expressed in HCC samples compared to adjacent non-tumor tissues. Higher DHX37 expression is correlated with various clinicopathological characteristics in HCC, including AFP, adjacent hepatic tissue inflammation, histologic grade, T stage, and pathologic stage. Survival analysis revealed that the high DHX37 group had significantly shorter overall survival (OS), progress-free interval (PFI), and disease-specific survival (DSS) compared to the low DHX37 group. By analyzing the correlation between DHX37 and the IC50 of chemotherapeutic drugs, the results showed that DHX37 expression level was negatively correlated with the IC50 of 11 chemotherapeutic drugs. Further analysis indicated that DHX37 and its co-expressed genes may play important roles in activating the cell cycle, DNA repair, chemokine signaling pathways, and regulating the immune response, which leads to a poor prognosis in HCC. High expression of DHX37 is an independent risk factor for poor prognosis in HCC, and DHX37 is expected to be a potential target to inhibit tumor progression. Targeting DHX37 may enhance chemotherapeutic drug sensitivity and immunotherapeutic efficacy in HCC.

Obstruction of bile ducts due to gallstones can lead to biliary acute pancreatitis (BAP). According to Perides et al., G protein-coupled bile acid receptor-1 (GPBAR1) mediates BAP. However, Zi's findings suggest that GPR39, rather than GPBAR1, mediates TLCAS-induced increases in cytosolic calcium and acinar cell necrosis, casting doubt on the role of GPBAR1 in BAP. Numerous G protein-coupled receptors on pancreatic acinar cells utilize Ca²⁺ and cyclic adenosine monophosphate (cAMP) as second messengers to manage pancreatic exocrine secretion, with significant cross-talk between these signals. The primary bile acid cholic acid (CA) and its conjugated forms are predominant in the human gallbladder. This study aimed to clarify the role and physiological significance of GPBAR1 by investigating the physiological and pathological effects of CA activation on GPBAR1 in pancreatic acinar cells. Isolated rat pancreatic acinar cells were treated with CA and CCK in vitro to observe the effect of CA-induced cAMP signaling on CCK-induced physiological and pathological calcium signaling. In vivo evaluations involved reverse biliopancreatic duct injections of 5 % sodium taurocholate (STC) or 5 % CA in rats. CA induced intracellular cAMP signaling in a concentration-dependent manner without increasing the intracellular Ca²⁺ concentration. CA did not independently cause calcium overload or enzyme activation, nor did it exacerbate calcium overload or enzyme activation from high-dose CCK. Reverse biliopancreatic duct injections of 5 % CA did not cause acute pancreatitis in the rats. Transcriptomic analysis revealed that 50 μM CA induced changes in gene expression related to protein synthesis in the endoplasmic reticulum and ribosomes. Furthermore, 50 μM CA accelerated the calcium waves and increased the enzyme secretion induced by CCK. GPBAR1 was found on the basolateral membrane in rat pancreatic tissue rather than near the apical region of acinar cells. GPBAR1 activation is not crucial for BAP activity but may play a role in bile acid regulation of pancreatic exocrine secretion, suggesting that GPBAR1 is a potential therapeutic target for pancreatic exocrine insufficiency.