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.  https://www.selleckchem.com/products/afuresertib-gsk2110183.html  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. 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. Anaerobic mild hypothermia increased the expression levels of Musashi‑1 and decreased the expression levels of NSE and NeuN in glial cells. The results of the present study demonstrated that bFGF, EGF and anaerobic mild hypothermia treatments may promote the transformation of glial cells into MSC‑like cells, and that the combination of these two treatments may have the optimal effect.Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non‑coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B‑cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT‑qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK‑8, clone formation, wound‑healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR‑495‑3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR‑495‑3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR‑495‑3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR‑495‑3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR‑495‑3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.