Background Ovarian cancer (OC) is one of the leading causes for cancer-related deaths among women. MicroRNAs (miRs) have been proved to be vital to the development and progression of OC. Hence, the study aims to evaluate the ability of miR-195-5p affecting cisplatin (DDP) resistance and angiogenesis in OC and the underlying mechanism. Methods MiRs that could target phosphoserine aminotransferase 1 (PSAT1), a differentially expressed gene in OC, were predicted by miRNA-mRNA prediction websites. The expression patterns of miR-195-5p in the OC tissues and cells were determined using RNA quantification assay. The role of miR-195-5p in OC was evaluated by determining DDP resistance, apoptosis and angiogenesis of OC cells after up-regulating or down-regulating miR-195-5p or PSAT1, or blocking the glycogen synthase kinase-3β (GSK3β)/β-catenin signaling pathway. Animal experiment was conducted to explore the effect of miR-195-5p on resistance to DDP and angiogenesis. Result MiR-195-5p directly targeted PSAT1 and down-regulated its expression. The expression of miR-195-5p was lower while that of PSAT1 was higher in OC tissues than in adjacent normal tissues. When miR-195-5p was over-expressed or PSAT1 was silenced, the expression of HIF-1α, VEGF, PSAT1, β-catenin as well as the extent of GSK3β phosphorylation was reduced, the angiogenesis and resistance to DDP was diminished and apoptosis was promoted both in vitro and in vivo. The inhibition of GSK3β/β-catenin signaling pathway was involved in the regulation process. Conclusion Over-expression of miR-195-5p reduced angiogenesis and DDP resistance in OC, which provides a potential therapeutic target for the treatment of OC.

Purpose: A long noncoding RNA called ZFPM2 antisense RNA 1 (ZFPM2-AS1) has been verified as a key modulator in multiple human cancer types. Nonetheless, the expression and functions of ZFPM2-AS1 in cervical cancer remain poorly understood. Therefore, our purpose was to characterize the expression pattern, clinical value, and detailed roles of ZFPM2-AS1 in cervical cancer. Methods: Reverse-transcription quantitative PCR was carried out to measure ZFPM2-AS1 expression in cervical cancer. A Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and a tumor xenograft experiment were conducted to determine the influence of ZFPM2-AS1 on cervical cancer cell proliferation, apoptosis, migration, and invasion in vitro and on tumor growth in vivo, respectively. Results: ZFPM2-AS1 was found to be aberrantly upregulated in cervical cancer, and its upregulation was associated with unfavorable values of clinical parameters. A ZFPM2-AS1 knockdown significantly reduced cervical cancer cell proliferation, migration, and invasion and increased apoptosis in vitro. The ZFPM2-AS1 knockdown decelerated tumor growth of cervical cancer cells in vivo. Molecular investigation indicated that ZFPM2-AS1 acts as a molecular sponge of microRNA-511-3p (miR-511-3p) in cervical cancer cells. Fibroblast growth factor receptor 2 (FGFR2) mRNA was validated as a direct target of miR-511-3p in cervical cancer, and its expression was positively modulated by ZFPM2-AS1. The effects of the ZFPM2-AS1 knockdown on malignant characteristics of cervical cancer cells were greatly attenuated by miR-511-3p inhibition. Conclusion: ZFPM2-AS1 promotes cervical cancer progression through upregulation of miR-511-3p-FGFR2 axis output, thereby pointing to possible diagnostics and therapeutics based on the ZFPM2-AS1-miR-511-3p-FGFR2 pathway.

In addition, co-author Beihua Kong stated that his name was added to the article without his knowledge and that he was neither aware of any contents of the article, nor the submission process. He also stated the email address provided on submission was not his email address, and that he did not sign any authorship form submitted to the journal.Author Beihua Kong agrees with this retraction. Author Peihai Zhang stated on behalf of remaining coauthors that they do not agree to this retraction.

Long noncoding RNA ZFPM2-AS1 enhances the malignancy of cervical cancer by functioning as a molecular sponge of microRNA-511-3p and consequently increasing FGFR2 expression. Cancer Manag Res. 2020;12:567-580.