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New Findings: What is the central question of this study?What are the morphological features and microRNA (miRNA) expression features of extracellular vesicles (EVs) from haemorrhoids (Hae‐EVs) and normal tissues? What are the potential functions of the differentially expressed (DE) miRNAs in Hae‐EVs?What is the main finding and its importance?We present, for the first time, the morphological features and miRNA profile of human Hae‐EVs. Four hundred and forty‐seven significant DE‐miRNAs were identified. Gene ontology and pathway analysis of the DE‐miRNAs indicated diverse roles of the Hae‐EVs through different pathways. Our findings provide EV‐based pathological features and the underlying mechanism of haemorrhoids. Extracellular vesicles (EVs) play important roles in many pathophysiologies as cell‐to‐cell communication vehicles. However, the features and potential functions of the EVs in haemorrhoids remain unclear. Therefore, we performed microRNA (miRNA) microarray analysis in EVs derived from haemorrhoid tissue to identify the profile of miRNAs in these EVs and predict their potential functions. We obtained typical EVs from both haemorrhoid and control tissues. Microarray analysis identified 447 miRNAs with significant differential expresssion (DE): 245 upregulated and 202 downregulated. The top three upregulated miRNAs in haemorrhoid EVs (Hae‐EVs), namely miR‐6741‐3p, miR‐6834‐3p and miR‐4254, were detected by RT‐qPCR in both Hae‐EVs and haemorrhoid tissues. Interestingly, we found a different expression pattern in the haemorrhoid tissues from that in Hae‐EVs. The potential target genes of these DE‐miRNAs were predicted by the miRWalk and miRDB databases. Gene ontology (GO) analysis of the target genes showed that the DE‐miRNAs contributed mainly to protein kinase activity, transcriptional activity and ubiquitin‐protein function. KEGG search found that the DE‐miRNAs might regulate the MAPK and Ras signalling pathways. These findings revealed, for the first time, the miRNA profiles in Hae‐EVs and provided potential targets and pathways involved in the pathological process. [ABSTRACT FROM AUTHOR]

RSK4 refers to one Ser/Thr protein kinase functioning downstream pertaining to the signaling channel of protein kinase (MAPK) stimulated by Ras/mitogen. RSK4 can regulate numerous substrates impacting cells' surviving state, growing processes and proliferating process. Thus, dysregulated RSK4 active state display a relationship to several carcinoma categories, covering breast carcinoma, esophageal squamous cell carcinoma, glioma, colorectal carcinoma, lung carcinoma, ovarian carcinoma, leukemia, endometrial carcinoma, and kidney carcinoma. Whether RSK4 is a tumor suppressor gene or one oncogene remains controversial. No specific inhibiting elements for RSK4 have been found. This review briefs the existing information regarding RSK4 activating process, the function and mechanism of RSK4 in different tumors, and the research progress and limitations of existing RSK inhibitors. RSK4 may be a potential target of molecular therapy medicine in the future. [ABSTRACT FROM AUTHOR]