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All the authors agreed that the article should be retracted. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 50 1821‑1831, 2017; DOI 10.3892/ijo.2017.3943].Long non‑coding RNAs (lncRNAs) have emerged as key players in the development and progression of cancer. FEZ family zinc finger 1 antisense RNA 1 (FEZF1‑AS1) is a novel lncRNA that is involved in the development of cancer and acts as a potential biomarker for cancer. However, the clinical significance and molecular mechanism of FEZF1‑AS1 in non‑small cell lung cancer (NSCLC) remains uncertain. In the present study, FEZF1‑AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC. Loss‑of‑function assays revealed that FEZF1‑AS1 inhibition decreased cell proliferation and migration, and arrested cells at the G2/M cell cycle phase. Mechanistically, FEZF1‑AS1 expression was influenced by N6‑methyladenosine (m6A) modification. Since FEZF1‑AS1 was mainly located in the cytoplasmic fraction of NSCLC cells, it was hypothesized that it may be involved in competing endogenous RNA regulatory network to impact the prognosis of NSCLC. Via integrating Arraystar Human mRNA microarray data and miRNA bioinformatics analysis, it was revealed that ITGA11 expression was decreased with loss of FEZF1‑AS1 and increased with gain of FEZF1‑AS1 expression, and microRNA (miR)‑516b‑5p inhibited the expression levels of both FEZF1‑AS and ITGA11. RNA‑binding protein immunoprecipitation and RNA pulldown assays further demonstrated that FEZF1‑AS1 could bind to miR‑516b‑5p and that ITGA11 was a direct target of miR‑516b‑5p by luciferase reporter assay. Overall, the present findings demonstrated that FEZF1‑AS1 was upregulated and acted as an oncogene in NSCLC by regulating the ITGA11/miR‑516b‑5p axis, suggesting that FEZF1‑AS1 may be a potential prognostic biomarker and therapeutic target for NSCLC.Hepatocellular carcinoma (HCC) is an invasive malignant neoplasm with a poor prognosis. The development of chemoresistance severely obstructs the chemotherapeutic efficiency of HCC treatment. Therefore, understanding the mechanisms of chemoresistance is important for improving the outcomes of patients with HCC. Eukaryotic translation initiation factor 5A2 (eIF5A2), which is considered to be an oncogene, has been reported to mediate chemoresistance in various types of cancer; however, its precise role in HCC remains unclear. Accumulating evidence has suggested that autophagy serves a dual role in cancer chemotherapy. The present study aimed to investigate the role of autophagy in eIF5A2‑mediated doxorubicin resistance in HCC. High expression levels of eIF5A2 in human HCC tissues were observed by immunohistochemistry using a tissue microarray, which was consistent with the results of reverse transcription‑quantitative PCR analysis in paired HCC and adjacent healthy tissues. HCC patient‑derived tumor xenograft mtherapy through a Beclin 1‑dependent pathway, and that eIF5A2 may be a novel potential therapeutic target for HCC treatment.Following the publication of the above article, the authors have realized that certain intended corrections were not carried over to the published version of the article. First, the description of the results of Figs. 5 and 6 did not match the figures; Edu and Transwell invasion assays were intended to have been excluded from the manuscript during the proofreading stage, although these data were presented in the description of the results for Figs. 5 and 6. Consequently, the text for the "circRNA_001275 promotes cell proliferation" subsection of the Results section towards the end of p. 153 should have read as follows "MTT assay was used to detect the effects of circRNA_001275 on cell proliferation. The results showed that cell viability was significantly increased in the circRNA_001275 OE group, and significantly decreased in the si circRNA_001275 group (both P less then 0.05, Fig. 5A and B), compared with the corresponding control groups." Furthermore, the text in the subsequent subsection ("circRNA_001275 .3892/ijo.2020.5050].Osteoarthritis is a chronic degenerative joint disease. Long non‑coding RNA plasmacytoma variant translocation 1 (PVT1) is involved in the progression of osteoarthritis and exosomes serve a central role in intercellular communication. However, whether PVT1 can be mediated by exosomes in osteoarthritis has not been reported. Whole blood was drawn from osteoarthritis patients and healthy volunteers. Lipopolysaccharide (LPS) was used to stimulate human normal chondrocytes (C28/I2) to construct a cell damage model in vitro. Protein levels were examined via western blot analysis. Bismuthsubnitrate eThe expression of PVT1, microRNA (miR)‑93‑5p and high mobility groupprotein B1 (HMGB1) was evaluated through reverse transcription‑quantitative PCR. Cell viability and apoptosis were determined through CCK‑8 or flow cytometric assay. Inflammatory cytokines were measured via ELISA. The relationship between PVT1 or HMGB1 and miR‑93‑5p was confirmed by dual‑luciferase reporter assay. PVT1, HMGB1 and exosomal PVT1 were upregulated while miR‑s treatment.Recently, the compilation of massive amounts of genetic and genomic information on a wide variety of human cancer types, collectively known as The Cancer Genome Atlas (TCGA), has revealed a wealth of descriptive classification schemes both within and between different types and sources of cancer. In endometrial cancer, TCGA analyses have produced a post hoc scheme composed of four clusters DNA polymerase ε catalytic subunit A (POLE) ultra‑mutated (cluster 1), microsatellite instability (MSI) hypermutated (cluster 2), copy‑number low (endometrioid, cluster 3) and copy‑number high (serous‑like, cluster 4). Given that cultured cells are the pre‑clinical platform of cancer research, it was questioned how representative endometrial cancer cultured cell lines are in the context of TCGA‑driven classification scheme. To address this issue in endometrial cancer cell lines, the present study investigated five commonly used cell lines Ishikawa, ECC‑1, Hec50co, KLE And RL95‑2. The histology, mutation profile, MutL homolog 1 promoter methylation, copy‑number variation, homologous recombination repair and microsatellite instability in each of these cell lines was assessed.