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Background: The expression of miR-141-3p in many malignant tumors has been verified. Nevertheless, the relationship between ovarian cancer and miR-141-3p remains undetermined. Therefore, further exploration is required. Results: According to data from 100 samples, the final results of RT-qPCR showed that miR-141-3p was highly expressed in ovarian cancer. Furthermore, miR-141-3p was able to distinguish ovarian cancer cells from ovary tissues. The most significant Kyoto Encyclopedia of Genes and Genomes pathway, was regulation of lipolysis in adipocytes in ovarian cancer. The expression of PIK3R1 was negatively correlated with miR-141- 3p. PIK3R1 has a combing site with miR-141-3p. Conclusions: This study examined the expression levels and mechanism of miR-141-3p in ovarian cancer for the first time. The results suggested that miR-141-3p may promote the occurrence of ovarian cancer by down-regulating PIK3R1.How to cite: Shi L, Sun H-J, Zeng J-J, et al. Evaluation of miR-141-3p over-expression in ovarian cancer. Electron J Biotechnol 2022;58. https://doi.org/10.1016/j.ejbt.2022.04.006

Purpose: Our purpose was to systematically appraise the clinicopathological significance and explore the molecular bases of CKS2 in endometrial carcinoma.Patients and Methods: We measured the clinicopathological significance of CKS2 using diverse methods of public RNA-seq, microarrays, and in-house tissue microarrays to investigate the molecular basis of CKS2 in endometrial carcinoma through upstream transcriptional analysis, immune infiltration correlation analysis, and co-expression analysis.Results: Both the analysis for public RNA-seq plus the microarray data and in-house tissue microarray confirmed the significant overexpression of CKS2 in a total of 1,021 endometrial carcinoma samples compared with 279 non-cancer endometrium samples (SMD = 2.10, 95% CI = 0.72–3.48). The upregulated CKS2 was significantly related to the lymph node metastasis and advanced clinical grade of endometrial carcinoma patients (p < 0.001). Mutation types such as amplification and mRNA occurred with high frequency in the CKS2 gene in endometrial carcinoma patients. A series of miRNAs and transcription factors, such as hsa-miR-26a, hsa-miR-130a, hsa-miR-30, E2F4, MAX, and GABPA, were predicted to regulate the transcription and expression of CKS2. Significant links were found between CKS2 expression and the infiltration level of B cells, CD4+ T cells, and neutrophils in endometrial carcinoma. CKS2-coexpressed genes were actively involved in pathways such as the mitotic cell cycle process, PID aurora B pathway, and prolactin signaling pathway.Conclusion: The overexpressed CKS2 showed positive correlations with the clinical progression of endometrial carcinoma and was associated with various cancer-related biological processes and pathways, showing potential as a promising clinical biomarker for endometrial carcinoma.