Normal placentation and successful maintenance of pregnancy depend on the successful migration and invasion of trophoblasts into maternal tissues. Previous studies reported that microRNAs (miRs) are expressed in trophoblasts, and can regulate their migration and invasion. The present study aimed to investigate miR‑181b‑5p function in HTR‑8/SVneo trophoblasts and explore its underlying mechanism in the pathogenesis of multiple abnormal trophoblast invasion‑related events. Reverse‑transcription quantitative PCR and western blotting were used to test the expression of miR‑181b‑5p and sphingosine‑1‑phosphate receptor 1 (S1PR1) in samples of multiple abnormal trophoblast invasion‑related events. Transwell invasion and wound healing assays were performed to determine cell invasion and migration abilities. A luciferase reporter assay was conducted to identify the downstream target of miR‑181b‑5p. Overexpression of miR‑181b‑5p suppressed HTR‑8/SVneo cell migration and invasion, whereas inhibition of miR‑181b‑5p induced an opposite effect. The S1PR1 gene was further identified as a novel direct target of miR‑181b‑5p. Specifically, miR‑181b‑5p bound directly to the 3'‑untranslated region of S1PR1 and suppressed its expression. Moreover, overexpression of S1PR1 reversed the inhibitory effect of miR‑181b‑5p. Taken together, ectopic expression of miR‑181b‑5p impaired the migration and invasion of trophoblasts by directly targeting S1PR1, thereby providing new insights into the pathogenesis of multiple abnormal trophoblast invasion‑related events.Congenital bilateral absence of the vas deferens (CBAVD) is predominantly caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CBAVD accounts for 2‑6% of male infertility cases and up to 25% of cases of obstructive azoospermia. With the use of pre‑implantation genetic diagnosis, testicular or epididymal sperm aspiration, intracytoplasmic sperm injection and in vitro fertilization, patients affected by CBAVD are able to have children who do not carry CFTR gene mutations, thereby preventing disease. Therefore, genetic counseling should be provided to couples receiving assisted reproductive techniques to discuss the impact of CFTR gene mutations on reproductive health. In the present article, the current literature concerning the CFTR gene and its association with CBAVD is reviewed.Long non‑coding RNAs (lncRNAs) have recently gained attention due to their important roles in human cancer types, such as breast and gastric cancer. The present study measured alterations in muskelin 1 antisense RNA (MKLN1‑AS) expression in hepatocellular carcinoma (HCC) and evaluated its clinical value in patients with HCC. Additionally, the current study investigated the effects of MKLN1‑AS on the malignant features of HCC cells. The detailed molecular mechanisms underlying the cancer‑promoting activities of MKLN1‑AS in HCC cells were also elucidated. MKLN1‑AS expression in HCC tissues and cell lines was detected using reverse‑transcription quantitative PCR (RT‑qPCR). Cell Counting Kit‑8 assays and flow cytometry were used to determine the roles of MKLN1‑AS in HCC cell proliferation and apoptosis. Migration and invasion assays, as well as tumor xenograft experiments were conducted to analyze migration and invasion in vitro and tumor growth in vivo, respectively. The interaction among microRNA‑654‑3p (miR‑65induced pro‑oncogenic effects during HCC progression by serving as a molecular sponge for miR‑654‑3p to increase HDGF expression. Therefore, the MKLN1‑AS/miR‑654‑3p/HDGF axis may offer a novel target for the diagnosis, prognosis, prevention and treatment of HCC.Infection by the severe acute respiratory syndrome (SARS) coronavirus‑2 (SARS‑CoV‑2) is the cause of the new viral infectious disease (coronavirus disease 2019; COVID‑19). Emerging evidence indicates that COVID‑19 may be associated with a wide spectrum of neurological symptoms and complications with central nervous system (CNS) involvement. It is now well‑established that entry of SARS‑CoV‑2 into host cells is facilitated by its spike proteins mainly through binding to the angiotensin‑converting enzyme 2 (ACE‑2). Preclinical studies have suggested that neuropilin‑1 (NRP1), which is a transmembrane receptor that lacks a cytosolic protein kinase domain and exhibits high expression in the respiratory and olfactory epithelium, may also be implicated in COVID‑19 by enhancing the entry of SARS‑CoV‑2 into the brain through the olfactory epithelium.  https://www.selleckchem.com/products/OSI027.html  In the present study, we expand on these findings and demonstrate that the NRP1 is also expressed in the CNS, including olfactory‑related regions such as the olfactory tubercles and paraolfactory gyri. This furthers supports the potential role of NRP1 as an additional SARS‑CoV‑2 infection mediator implicated in the neurologic manifestations of COVID‑19. Accordingly, the neurotropism of SARS‑CoV‑2 via NRP1‑expressing cells in the CNS merits further investigation.Previous studies have shown that (GM3), a ganglioside, suppresses hepatoma cell motility and migration by inhibiting phosphorylation of EGFR and the activity of the PI3K/AKT signaling pathway. Therefore, the aim of the present study was to investigate whether the combined treatment of CD82 with gangliosides can exert a synergistic inhibitory effect on cell motility and migration. Epidermal growth factor receptor (EGFR) signaling was studied for its role in the mechanism through which CD82 and gangliosides synergistically inhibit the motility and migration of SW620 human colon adenocarcinoma cells. GM3 and/or GM2 treatment, and/or overexpression of CD82 was performed in SW620 cells. High-performance thin layer chromatography, reverse transcription-quantitative PCR, western blotting and flow cytometry assays were used to confirm the content changes of GM2, GM3 and CD82. In addition, the phosphorylation of EGFR, MAPK and Akt were evaluated by western blot analysis. SW620 cell motility was investigated using wound healing analysis and chemotaxis migration assay.