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Ankylosing spondylitis (AS) is a chronic inflammatory disease. Transcriptional regulation of fibroblast growth factor 21 (FGF21) by the transcription factor Krüppel‑like factor 4 (KLF4) serves an important role in chronic inflammatory disease. However, to the best of our knowledge, the role of both these factors in AS has not been previously reported. In the present study, ATDC5 cells were induced by lipopolysaccharide (LPS) to establish an AS inflammatory injury model. The expression levels of FGF21 and KLF4 were detected using reverse transcription‑quantitative PCR and western blotting. Cell transfection was performed to alter the expression levels of KLF4 and FGF21. Subsequently, the regulatory effects and mechanisms underlying KLF4 and FGF21 on oxidative stress and inflammation in AS were investigated by performing Cell Counting Kit‑8 assays, ELISAs, TUNEL staining and western blotting. Moreover, the expression levels of sirtuin 1 (SIRT1)/NF‑κB/p53 pathway‑related proteins were detected via western blotting. FGF21 overexpression promoted LPS‑induced viability on ATDC5 cells, inhibited LPS‑induced apoptosis, and decreased the LPS‑induced inflammatory response and oxidative stress levels of ATDC5 cells. Overexpression of the transcription factor KLF4 reversed the protective effect of FGF21 overexpression on LPS‑induced inflammatory injury in ATDC5 cells. The results suggested that this process may be achieved via regulating the SIRT1/NF‑κB/p53 signaling pathway. Overall, the present study demonstrated that KLF4 downregulates FGF21 to activate inflammatory injury and oxidative stress of LPS‑induced ATDC5 cells via SIRT1/NF‑κB/p53 signaling.Hepatocellular carcinoma (HCC) is a malignant tumor with a high metastatic rate. Recent studies have shown that the mitosis‑associated spindle‑assembly checkpoint regulatory protein spindle pole body component 25 homolog (SPC25) promotes HCC progression, although the underlying mechanism has yet to be fully elucidated. The aim of the present study was to investigate the mechanism through which SPC25 may promote HCC progression in greater detail. First, the expression of SPC25 was analyzed in publicly available databases to explore the association between SPC25 and HCC metastasis. Western blotting was subsequently performed to examine the level of SPC25 expression in different HCC cell lines. SPC25 was then silenced in HCCLM3 and Huh7 cells, and the effects of SPC25 silencing were investigated using cell proliferation, wound‑healing, Transwell migration assays and an in vivo mouse model. Finally, the mechanism of SPC25 action with respect to the promotion of HCC metastasis was explored using microarray analysiic indicator and as a promoter of metastasis in HCC, and the underlying mechanism of its action has been partially elucidated, suggesting that SPC25 could be used as a biomarker and as a target for therapeutic intervention in the treatment of HCC.Osteoarthritis (OA), although extensively researched, still lacks an effective and safe treatment. The only current treatment option available for advanced OA is joint replacement surgery. This surgery may pose the risks of persistent pain, surgical complications and limited implant lifespan. Transforming growth factor (TGF)‑β has a crucial role in multiple cellular processes such as cell proliferation. Any deterioration in TGF‑β signaling pathways can have an immense impact on OA. Owing to the crucial role of TGF‑β in cartilage homeostasis, targeting it could be an alternative therapeutic approach. Additionally, stem cell‑based therapy has recently emerged as an effective treatment strategy that could replace surgery. A number of recent findings suggest that the tissue regeneration effect of stem cells is attributed to the paracrine secretion of anti‑inflammatory and chondroprotective mediators or trophic factors, particularly nanosized extracellular vesicles (i.e., exosomes). Literature searches were performed in the MEDLINE, EMBASE, Cochrane Library and PubMed electronic database for relevant articles published before September 2021. Multiple investigators have confirmed TGF‑β3 as a promising candidate which has the chondrogenic potential to repair articular cartilage degeneration. Combining TGF‑β3 with bone morphogenetic proteins‑6, which has synergistic effect on chondrogenesis, with an efficient platform such as exosomes, which themselves possess a chondroprotective function, offers an innovative and more efficient approach to treat injured cartilage. In addition, multiple findings stating the role of exosomes in chondroprotection has also verified a similar fact showing exosomes may be a more favorable choice than the source itself. In the present review, the importance of TGF‑β family in OA and the possibility of therapeutic treatment using stem cell‑derived exosomes are described.The role of mast cells in colorectal cancer (CRC) has been an area of intense interest. Mast cell density is closely related to CRC development and prognosis. The identification of mast cell progenitors (MCps) in peripheral blood provides an opportunity to explore the frequency and distribution of mast cells in the circulation and tumour microenvironment of patients with CRC at different disease stages. The aim of the presents study was to investigate the changes of MCps and mast cells in CRC. Flow cytometry was used to measure the circulating frequency of MCps in 37 patients with CRC and 12 healthy control (HC) patients, and the frequency of mast cells in tissue from 15 patients with CRC and 7 patients with haemorrhoids. In the present study, lower levels of circulating MCps in patients with CRC were found, which was significantly related to CRC development. After surgery, the frequency of circulating MCps was significantly increased. However, the frequency of mast cells in tumour tissues was lower than that in adjacent normal tissues and compared with HC tissues and was not associated with CRC progression.The tumor suppressive role of CYLD lysine 63 deubiquitinase (CYLD) is known in melanoma. To the best of our knowledge, however, the precise mechanism underlying the tumor suppressive function of CYLD has yet to be clarified. In the present study, a novel melanoma mouse model was generated, which revealed accelerated tumor growth in Cyld‑knockout (Cyld‑/‑) compared with Cyld‑wild‑type (Cyld+/+) mice. To determine the underlying molecular mechanism, mutation analysis of primary tumor‑derived cell lines from Cyld+/+ and Cyld‑/‑ mice was performed using RNA sequencing data. Variant calling revealed no common mutations in Cyld‑/‑ compared with Cyld+/+ cells. Thus, the epigenetic processes influencing development and progression of melanoma were investigated. Initial analysis of expression pattern of known hypermethylated genes in melanoma (suppressor of cytokine signalling, methylthioadenosine phosphorylase, cadherin 1) in the presence or absence of 5'‑Aza‑deoxyctidine treatment revealed that CYLD does not play a key role in DNA methylation. Chromatin accessibility and histone H3 modification assay uncovered a role of CYLD in the formation of chromatin structure. Subsequent inhibitor experiments confirmed the effect of CYLD on H3K9me2 level associated with heterochromatin. Furthermore, enhanced H3K9 dimethylation in Cyld‑/‑ melanoma cells was associated with upregulation of euchromatic histone lysine methyltransferase 2 (EHMT2). Moreover, the specific inhibitor of EHMT2, CM272, resulted in decreased proliferation and relaxation of compact chromatin in Cyld‑deficient melanoma cells. These results reveal a novel role of CYLD in histone methylation and chromatin packaging.Subsequently to the publication of the above article, an interested reader drew to the authors' attention that certain of the data panels featured in Figs. 1B, 4A, 6A and 8A, showing DAPI or NAC staining of the cells, appeared to contain overlapping data. The authors have consulted their original data, and realize that errors were made during the compilation of these figures; consequently, they have repeated the affected experiments. The revised versions of Figs. 1, 4, 6 and 8, featuring replacement data for Figs. 1B, 4A, 6A and 8A, are shown on the subsequent pages. The authors regret the errors that were made during the preparation of the published figures, and confirm that these errors did not affect the conclusions reported in the study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 36 205‑214, 2016; DOI 10.3892/or.2016.4812].Survivin is overexpressed in various cancers and is correlated with treatment resistance and prognosis. MicroRNAs (miRNAs) directly regulate several target genes and are potential therapeutic agents for various cancers. The present study evaluated multiple gene targets of miR‑218, including survivin, in osteosarcoma and compared the anti‑tumor effects of miR‑218 with those of YM155, an anti‑survivin agent. It assessed the expression levels of miR‑218 and survivin in osteosarcoma and osteoblast cell lines, as well as the proliferative, migratory and invasive capacities of cells following treatment with miR‑218 or YM155. selleck products The form of cell death was assessed using fluorescence‑activated cell sorting analysis to examine the expression of invasion ability‑related genes. Osteosarcoma cell lines were subcutaneously injected into immunodeficient mice; the mice were then treated with miR‑218 or YM155 to assess the anti‑tumor effects of these agents. The results showed that miR‑218 was downregulated, whereas survivin was overexpressed in the osteosarcoma cell line compared with normal osteoblast cells. The expression of survivin was suppressed upon overexpression of miR‑218 (miR‑218 group) or administration of YM155 (YM155 group), leading to apoptosis and inhibition of osteosarcoma cell proliferation. Invasion and migration abilities were inhibited in the miR‑218 group, but not in the YM155 group. In the animal model, both the miR‑218 and YM155 groups showed a reduced tumor volume and decreased survivin expression. In osteosarcoma, miR‑218 showed a wider range of therapeutic efficacy compared with YM155, suggesting that miR‑218 should be evaluated as a treatment target.Subsequently to the publication of this paper, an interested reader drew to the authors' attention that Figs. 3 (showing how PKG II overexpression inhibits the migration of various types of cancer cells) and 6 (showing representative photomicrographs of apoptotic cells under different experimental conditions at x200 magnification) contained apparently duplicated data panels within the figures. After having examined their original data, the authors have realized that these figures were inadvertently assembled incorrectly; specifically, the data shown in the HepG2-Ad-LacZ+EGF and OS-RC-2-Ad-LacZ+EGF panels in Fig. 3A and the HepG2-Ad-LacZ+cGMP+EGF, OS-RC-2-Ad-PKGII+cGMP+EGF and U251-Ad-PKGII+cGMP+EGF panels in Fig. 6A were selected incorrectly. The corrected versions of Figs. 3 and 6 are shown on the next two pages. Note that these errors did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this and apologize to the readership for any inconvenience caused.