Gastric cancer (GC) is the third leading cause of cancer‑related mortality and the fifth most common type of cancer worldwide. GC stem cells (GCSCs) have been reported to be responsible for the malignant behavior of GC. However, the key molecular mechanism controlling GCSC function remains unclear. The present study aimed to investigate the function of retinoic acid‑related orphan receptor β (RORβ) in GC. The expression levels of RORβ in GC cells and clinical GC tissues were analyzed using western blotting, reverse transcription‑quantitative PCR (RT‑qPCR) and immunohistochemistry. The association between RORβ expression levels and GCSC markers was analyzed using Gene Set Enrichment Analysis, and GeneChip was performed to identify differentially expressed genes between control and RORβ‑overexpressing GC cells. CCK‑8 and flow cytometric assays were used to evaluate the effect of RORβ on cell viability and apoptosis, respectively. The effect of RORβ on the self‑renewal capacity of GCSCs was measured using a sphe decrease the activity of the Wnt/β‑catenin signaling pathway in GCSCs. In conclusion, the findings of the present study identified RORβ as a novel suppressor of GCSCs and highlighted the prospect of RORβ as a novel candidate target for stem cell‑based GC therapy.Renal cell carcinoma (RCC) is a major healthcare burden globally. Tumor‑derived extracellular vesicles (EVs) contribute to the formation of a pro‑metastatic microenvironment. In the present study, we explored the role and mechanism of RCC cell 786‑O‑derived EVs (786‑O‑EVs) in RCC. First, 786‑O‑EVs were extracted and identified, and EV internalization of RCC cells was observed. RCC cell malignant behaviors and long noncoding RNA (lncRNA) metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) expression patterns were detected before and after 786‑O‑EV treatment. MALAT1 was intervened to evaluate RCC cell behaviors. The downstream mechanism involving MALAT1 was predicted. In addition, the relationship among MALAT1, transcription factor CP2 like 1 (TFCP2L1) and ETS proto‑oncogene 1, transcription factor (ETS1) was analyzed. TFCP2L1 expression patterns were measured after 786‑O‑EV exposure. Tumor xenograft formation assay and lung metastasis model were adopted to verify the role of 786‑O‑EVs in vivo in RCC. It was found that 786‑O‑EVs could be internalized by RCC cells. 786‑O‑EVs promoted RCC cell malignant behaviors, accompanied by elevated MALAT1 expression levels. The 786‑O‑EVs with MALAT1 knockdown attenuated the promotive effect of sole 786‑O‑EVs on RCC cells. MALAT1 located ETS1 in the TFCP2L1 promoter and negatively regulated TFCP2L1, and ETS1 protein could specifically bind to MALAT1. 786‑O‑EVs enhanced the binding of ETS1 and the TFCP2L1 promoter and decreased TFCP2L1 expression. In vivo, 786‑O‑EVs promoted tumor growth and RCC lung metastasis, which was suppressed following inhibition of MALAT1. Our findings indicated that 786‑O‑EVs promoted RCC invasion and metastasis by transporting MALAT1 to promote the binding of transcription factor ETS1 and TFCP2L1 promoter.Following the publication of this paper, it was drawn to the Editors’ attention by a concerned reader that certain of the Transwell migration assay data shown in Fig. 4D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 33 1115‑1122, 2015; DOI 10.3892/or.2015.3734].Following the publication of the above article, an interested reader drew to the authors’ attention that they had mentioned that activated PKCδ phosphorylates IKKβ in order that IKKβ is relocated to the plasma membrane, resulting in the induction of mast cell degranulation; however, four references the authors had included did not seem to support this statement. The authors have re-examined their paper, and realized that the four references the reader mentioned were indeed cited incorrectly, and wish to rectify this error through revising the third paragraph in the Discussion section, the References section, and an associated figure (Fig. 6C) in order to avoid any further misunderstandings on the part of the readership. First, the authors wish to revise the wording of the third and fourth paragraphs of the Discussion, as featured on pp. 1101-1102, to the following (changed text is indicated in bold) ‘We showed that CRT exerts anti-AD effect through inhibition of the mast cell degranulation in mast cells. Upon the readers, and the corrected version of Fig. 6 appears on the next page. All these corrections have been approved by all the authors, with the exception of the first author, Sumiyasuren Buyanravjikh, who is no longer uncontactable. The authors regret that these errors were included in the paper, even though they did not substantially alter any of the major conclusions reported in the study, are grateful to the Editor for allowing them this opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. Veliparib [the original article was published in Molecular Medicine Reports 18 1095‑1193, 2018; DOI 10.3892/mmr.2018.9042].Recent studies have found that somatic gene mutations and environmental tumor‑promoting factors are both indispensable for tumor formation. Telomeric repeat‑binding factor (TRF)2 is the core component of the telomere shelterin complex, which plays an important role in chromosome stability and the maintenance of normal cell physiological states. In recent years, TRF2 and its role in tumor formation have gradually become a research hot topic, which has promoted in‑depth discussions into tumorigenesis and treatment strategies, and has achieved promising results. Some cells bypass elimination, due to either aging, apoptosis via mutations or abnormal prolongation of the mitotic cycle, and enter the telomere crisis period, where large‑scale DNA reorganization occurs repeatedly, which manifests as the precancerous cell cycle. Finally, at the end of the crisis cycle, the mutation activates either the expression level of telomerase or activates the alternative lengthening of telomere mechanism to extend the local telomeres.