Background. The purpose of this study was to explore the functions of FOXD2-AS1 and miR-31 in retinoblastoma. Material and Methods. An RT-qPCR assay was applied to calculate the mRNA levels of FOXD2-AS1, miR-31, and PAX9. A dual-luciferase reporter gene assay was employed to verify the connection between FOXD2-AS1, miR-31, and PAX9 expression. Results. FOXD2-AS1 was upregulated, and miR-31 was lowly expressed in retinoblastoma. Low expression of FOXD2-AS1 promoted cell proliferation and migration, and upregulation of FOXD2-AS1 inhibited proliferative and migratory abilities. lncRNA FOXD2-AS1 directly bound to miR-31 and regulated miR-31 expression in SO-RB50 cells. Cell proliferation and migration were inhibited by the miR-31 mimic. miR-31 mediated PAX9 expression via directly binding to PAX9 mRNA. A miR-31 inhibitor partially reversed the effect of FOXD2-AS1 knockdown on the proliferation and migration in SO-RB50 cells. FOXD2-AS1 knockdown reduced PAX9 expression in SO-RB50 cells. PAX9 had negative connection with miR-31, and it had positive relationship with FOXD2-AS1. Conclusion. lncRNA FOXD2-AS1 inhibited cell proliferation and migration via the miRNA-31/PAX9 axis in retinoblastoma.

To detect LINC00565 expression level in endometrial carcinoma (EC) samples and cell lines, and the correlations between LINC00565 and clinical features of EC patients. After intervening LINC00565, the underlying mechanism about proliferative ability in EC cell lines is observed. Methods: Relative levels of LINC00565 and KLF9 in 52 paired EC and paracancerous tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between relative level of LINC00565 or KLF9 and clinical features of EC patients was analyzed. After knockdown of LINC00565 and KLF9, potential regulations of them on biological functions of EC were examined by Cell Counting Kit (CCK-8), colony formation assay and in vivo xenograft model in nude mice, respectively. At last, dualluciferase reporter assay and rescue experiments were conducted to illustrate the mechanisms of LINC00565 and KLF9 in mediating the development of EC. Results: LINC00565 was upregulated in EC tissues. Chi-square analysis showed that a high level of LINC00565 predicted large tumor size, advanced pathological staging and poor prognosis in EC. Silence of LINC00565 decreased proliferative ability in EC cells and tumor growth in nude mice bearing EC. KLF9 was the target gene of LINC00565. The negative interaction between LINC00565 and KLF9 was responsible for stimulating the malignant development of EC. Knockdown of KLF9 could abolish the regulatory effects of silenced LINC00565 on proliferative ability and tumorigenesis in EC. Conclusion: LINC00565 is upregulated in EC tissues and closely linked to tumor size, pathological staging and poor prognosis in EC patients. LINC00565 stimulates proliferative ability in EC by downregulating KLF9.

At the authors request, the Editor and Publisher of OncoTargets and Therapy are retracting the published article. The authors informed the journal that they were unable to verify the reported findings and requested to retract the article. The Editor agreed with the author's request.We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as "Retracted".