As a non-coding RNA molecule, circular RNAs (circRNAs) have significant specificity, and existing data suggest a close relationship between them and the prognosis of patients with gastric cancer (GC). However, this mechanism has no evidence yet. This article explores the functions of hsa_circRNA_102415 in the malignant behavior and potential downstream signaling of GC cells. The chosen approach is loss of signal and functional gain.

To investigate and analyze the relationship between hsa_circRNA_102415 and GC and explore its specific role. Results provide reference for other researchers to develop targeted treatment plans.

The gene expression omnibus (GEO) database can be used to obtain the microarray dataset GSE83521. Data were analyzed using the GEO2R tool to identify differences in circRNAs between normal and GC samples. Quantitative real-time polymerase chain reaction was used to detect differentially expressed genes in GC tissue samples and adjacent cancer tissue samples. GC cells were transfected with small interfering-hsa_circRNA_104415 and plasmid DNA (pcDNA)-hsa_ircRNA_102415. Multiple detection methods, such as Transwell and cell counting kit 8, were used to evaluate cellular physiological activities, including cell invasion and proliferation. The relationship between Wnt family members 2B, microRNA (miR)-4529-5p, etc., including argonaute 2-RNA immunoprecipitation and luciferase reporter genes was analyzed. Rescue experiments were conducted to analyze and explore the relationship between the malignant behavior of GC cells and hsa_circRNA_102415.

GEO2R analysis confirmed that hsa_circRNA_102415 had significantly higher expression levels in disease tissues. hsa_circRNA_102415 and miR-4529-5p showed a negative correlation in disease cells, suggesting that hsa_circRNA_102415 upregulated WNT2B expression in GC cells as a competing endogenous RNA for miR-4529-5p. miR-4529-5p mimic or small interfering-WNT2B reversed the effects of pcDNA-hsa_circRNA_102415 or miR-4529-5p inhibitor on cell malignant functions.

miR-4529-5p was used to successfully activate the potential of WNT2B, clarify the role of hsa_circRNA_102415 in GC cells, and provide reference for other researchers to develop targeted treatment plans.

Oculomotor nerve palsy (ONP) is a neuroparalytic disorder resulting in dysfunction of innervating extraocular muscles (EOMs), of which the pathological characteristics remain underexplored.

In this study, medial rectus muscle tissue samples from four ONP patients and four constant exotropia (CXT) patients were collected for RNA sequencing. Differentially expressed circular RNAs (circRNAs) were identified and included in functional enrichment analysis, followed by interaction analysis with microRNAs and mRNAs as well as RNA binding proteins. Furthermore, RT-qPCR was used to validate the expression level of the differentially expressed circRNAs.

A total of 84 differentially expressed circRNAs were identified from 10,504 predicted circRNAs. Functional enrichment analysis indicated that the differentially expressed circRNAs significantly correlated with skeletal muscle contraction. In addition, interaction analyses showed that up-regulated circRNA_03628 was significantly interacted with RNA binding protein AGO2 and EIF4A3 as well as microRNA hsa-miR-188-5p and hsa-miR-4529-5p. The up-regulation of circRNA_03628 was validated by RT-qPCR, followed by further elaboration of the expression, location and clinical significance of circRNA_03628 in EOMs of ONP.

Our study may shed light on the role of differentially expressed circRNAs, especially circRNA_03628, in the pathological changes of EOMs in ONP.

Tumor cell invasiveness and metastasis are the main causes of mortality in cancer. Tumor progression is composed of many steps, including primary tumor growth, local invasion, intravasation, survival in the circulation, pre-metastatic niche formation, and metastasis. All these steps are strictly controlled by microRNAs (miRNAs), small non-coding RNA that regulate gene expression at the post-transcriptional level. miRNAs can act as oncomiRs that promote tumor cell invasion and metastasis or as tumor suppressor miRNAs that inhibit tumor progression. These miRNAs regulate the actin cytoskeleton, the expression of extracellular matrix (ECM) receptors including integrins and ECM-remodeling enzymes comprising matrix metalloproteinases (MMPs), and regulate epithelial-mesenchymal transition (EMT), hence modulating cell migration and invasiveness. Moreover, miRNAs regulate angiogenesis, the formation of a pre-metastatic niche, and metastasis. Thus, miRNAs are biomarkers of metastases as well as promising targets of therapy. In this review, we comprehensively describe the role of various miRNAs in tumor cell migration, invasion, and metastasis.

Gastric cancer (GC) is a malignant tumor with high morbidity and mortality in the world. Circular RNA hsa_circHN1_005 (circ_HN1), also termed as hsa_circ_0045602, is reported as an oncogene in GC. However, the molecular mechanism of circ_HN1 in GC development has not been fully explored. Here, we surveyed the regulatory mechanism of circ_HN1 in GC progression. The levels of circ_HN1, miR-302b-3p, and rho-associated coiled-coil containing protein kinase 2 (ROCK2) mRNA were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, colony formation, cell cycle progresion, migration, and invasion were determined by using cell counting, flow cytometry, colony formation, or transwell assays. Protein levels were detected with Western blotting. The relationship between circ_HN1 or ROCK2 and miR-302b-3p was verified via dual luciferase reporter or RNA immunoprecipitation (RIP) assays. The role of circ_HN1 in vivo was confirmed by xenograft assay. We observed that circ_HN1 and ROCK2 were upregulated while miR-302b-3p was downregulated in GC tissues and cells. Circ_HN1 silencing slowed tumor growth in vivo and impeded cell proliferation migration, invasion, and facilitated cell apoptosis in GC cells in vitro. Circ_HN1 sponged miR-302b-3p to regulate ROCK2 expression. MiR-302b-3p inhibitor reversed circ_HN1 silencing-mediated influence on the malignant behaviors of GC cells. Furthermore, ROCK2 overexpression restored miR-302b-3p mimic-mediated impacts on cell malignant behaviors in GC cells. In conclusion, circ_HN1 exerted an oncogenic role in GC through upregulating ROCK2 via sponging miR-302b-3p, offering evidence that circ_HN1 is a potential target for GC therapy.