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In addition, the protein expression levels of MMP13 were significantly increased in OA tissues and IL‑1β‑treated CHON‑001 cells compared with the controls. SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase‑3 and p21 in IL‑1β‑treated CHON‑001 cells. In addition, IL‑1β induced CHON‑001 cell apoptosis, while SNHG16 knockdown decreased IL‑1β‑induced apoptosis. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR‑373‑3p in OA. Finally, the results suggested that the proinflammatory effect of IL‑1β on CHON‑001 cells was significantly reduced by SNHG16 knockdown. In conclusion, lncRNA SNHG16 knockdown significantly limited the progression of OA by sponging miR‑373‑3p in vitro, which suggested that SNHG16 may serve as a potential therapeutic target for OA.Accumulating evidence indicates that long non‑coding RNAs (lncRNAs) may serve essential roles during tumorigenesis of colorectal cancer (CRC). The lncRNA ZFPM2‑AS1 was observed to be involved in the progression of numerous types of cancer, such as lung adenocarcinoma and cervical cancer. The aim of the present study was to investigate the expression levels and function of ZFPM2‑AS1 in CRC. Expression levels of ZFPM2‑AS1 in tissue and CRC cells were measured by reverse transcription‑quantitative PCR. Furthermore, cell proliferation and Transwell assays were conducted to investigate the functional role of ZFPM2‑AS1 in vitro. In addition, bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation assay and western blotting were performed to explore the possible underlying mechanism. The expression levels of ZFPM2‑AS1 were significantly upregulated in tissue samples from patients with CRC and CRC cell lines compared with normal tissue and normal human colorectal mucosa cell line. Notably, the upregulation of ZFPM2‑AS1 was significantly associated with tumor size, histological differentiation, lymph node metastasis and TNM stage. In addition, ZFPM2‑AS1 knockdown significantly inhibited cell proliferation, migration and invasion compared with the control group in vitro. Moreover, it was found that ZFPM2‑AS1 positively regulated tripartite motif containing 24 (TRIM24) expression by sponging miR‑137. In conclusion, the present study indicated that ZFPM2‑AS1 may serve as an oncogene in CRC by regulating the miR‑137/TRIM24 axis.The present study explored the association of long non‑coding RNA (lncRNA) antisense non‑coding RNA in the INK4 locus (ANRIL) with the development of acute myeloid leukemia (AML) clinical features and prognosis of patients with AML. Bone marrow mononuclear cells (BMMCs) were obtained from 178 patients with de novo AML prior to initial therapy and from 30 healthy donors. The expression of lncRNA ANRIL in BMMCs was detected by reverse transcription‑quantitative PCR. Complete remission (CR) was assessed after induction therapy. Event‑free survival (EFS) and overall survival (OS) were evaluated during the follow‑up. The levels of lncRNA ANRIL were increased in patients with AML compared with those in healthy donors and were capable of distinguishing patients with AML from healthy donors (area under the curve, 0.886; 95% CI, 0.820‑0.952). Furthermore, lncRNA ANRIL was associated with an increased occurrence internal tandem duplications in the FMS‑like tyrosine kinase 3, decreased occurrence inv(16) or t(16;6), intet for AML.Acute progressive hypoxic respiratory failure caused by various predisposing factors is known as acute respiratory distress syndrome (ARDS). Although penehyclidine hydrochloride (PHC), an anticholinergic drug, is widely applied in clinical practice, the specific mechanisms underlying PHC in the treatment of ARDS are not completely understood. In the present study, BEAS‑2B cells were treated with 10 ng/ml lipopolysaccharide (LPS) to establish an ARDS cell model and a rat model of acute lung injury (ALI). The influences of PHC and/or autophagy inhibitor (3‑methyladenine (3‑MA)) on the morphology, autophagy, proliferation and apoptosis of cells and tissues were evaluated using hematoxylin and eosin staining, Cell Counting Kit‑8 assays, Hoechst staining, TUNEL staining, flow cytometry, immunofluorescence assays, ELISAs and scanning electron microscopy. The expression levels of apoptosis‑ and autophagy‑related proteins were measured via western blotting. The results indicated that PHC enhanced proliferation and autophagy, and decreased apoptosis and the inflammatory response in LPS‑induced BEAS‑2B cells and ALI model rats. In addition, 3‑MA reversed the effects of PHC on proliferation, inflammation, apoptosis and autophagy in LPS‑induced BEAS‑2B cells. Therefore, the present study suggested that PHC demonstrated a protective effect in LPS‑induced ARDS by regulating an autophagy‑related pathway.Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an in vivo study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (Il6) and programmed cell death 1 (Pdcd1) in blood exhibited significant and positive correlations with the severity of DICT. In an in vitro study using cardiomyocyte H9c2 cells, knockdown of Il6 or Pdcd1 by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of Il6 and Pdcd1 in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for Il6 and Pdcd1 mRNA expression in DICT.Understanding the molecular and cellular processes in skin wound healing can pave the way for devising innovative concepts by turning the identified natural effectors into therapeutic tools. Based on the concept of broad‑scale engagement of members of the family of galactoside‑binding lectins (galectins) in pathophysiological processes, such as cancer or tissue repair/regeneration, the present study investigated the potential of galectins‑1 (Gal‑1) and ‑3 (Gal‑3) in wound healing. Human dermal fibroblasts, which are key cells involved in skin wound healing, responded to galectin exposure (Gal‑1 at 300 or Gal‑3 at 600 ng/ml) with selective changes in gene expression among a panel of 84 wound‑healing‑related genes, as well as remodeling of the extracellular matrix. In the case of Gal‑3, positive expression of Ki67 and cell number increased when using a decellularized matrix produced by Gal‑3‑treated fibroblasts as substrate for culture of interfollicular keratinocytes. In vivo wounds were topically treated with 20 ng/ml Gal‑1 or ‑3, and collagen score was found to be elevated in excisional wound repair in rats treated with Gal‑3. The tensile strength measured in incisions was significantly increased from 79.5±17.5 g/mm2 in controls to 103.1±21.4 g/mm2 after 21 days of healing. These data warrant further testing mixtures of galectins and other types of compounds, for example a combination of galectins and TGF‑β1.Subsequently to the publication of this paper, the authors have realized that Figs. 2 and 5 have been published containing the same GAPDH control protein bands. After having examined the final proofs of this article, the control blots were indeed different comparing between the figures, and regrettably an error concerning Fig. 2 was made during the final stages of the proof preparation. The corrected version of Fig. 2, including the correct GAPDH protein bands, is shown opposite. Note that the error that occurred with this Figure during production process did not affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The Editor of Molecular Medicine Reports apologizes to the authors and to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 19 927-934, 2019; DOI 10.3892/mmr.2018.9759].Colorectal cancer (CRC) is one of the most common types of malignancy and the third most commonly diagnosed form of cancer worldwide, ranking as the fourth leading cause of cancer‑associated mortality. read more MicroRNA (miR)‑576‑5p has been reported to be highly expressed in patients with CRC; however, its biological role remains unclear. The present study aimed therefore to investigate the biological role and underlying mechanism of miR‑576‑5p in CRC cell line SW480. The viability of SW480 cells following transfection with miR‑576‑5p mimic or inhibitor was analyzed using MTT assay. Wound healing and Transwell assays were performed to determine the cell migratory and invasive abilities, respectively. A dual luciferase reporter assay was used to verify the predicted binding site between miR‑576‑5p and Wnt5a. Reverse transcription‑quantitative PCR and western blotting were used to analyze the expression levels of miR‑576‑5p, E‑cadherin, N‑cadherin, vimentin, Snail1, Wnt5a, β‑catenin, c‑myc, cyclin D1 and p/t‑c‑Jun. Usi, providing a potential therapeutic target for the treatment of CRC.The transformation of rat primary glial cells into mesenchymal stem cells (MSCs) is intriguing as more seed cells can be harvested. The present study aimed to evaluate the effects of growth factors, hypoxia and mild hypothermia on the transformation of primary glial cells into MSCs. Rat primary glial cells were induced to differentiate by treatment with hypoxia, mild hypothermia and basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF). Immunohistochemistry and western blotting were then used to determine the expression levels of glial fibrillary acidic protein (GFAP), nestin, musashi‑1, neuron specific enolase (NSE) and neuronal nuclei (NeuN), in each treatment group. bFGF and EGF increased the proportion of CD44+ and CD105+ cells, while anaerobic mild hypothermia increased the proportion of CD90+ cells. The combination of bFGF and EGF, and anaerobic mild hypothermia increased the proportion of CD29+ cells and significantly decreased the proportions of GFAP+ cells and NSE+ cells. Treatment of primary glial cells with bFGF and EGF increased the expression levels of nestin, Musashi‑1, NSE and NeuN.