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FGFR4 silencing partially reversed EMT progression and FGFR4 this effect was enhanced in the presence of XAV939 (a β‑catenin inhibitor). The current data suggest that FGFR4 may be associated with prognosis in patients with colorectal cancer. In vitro functional tests revealed that FGFR4 may represent an effective therapeutic target for colorectal cancer. FGFR4 may also regulate EMT via the Wnt/β‑catenin pathway.Bone morphogenetic proteins (BMP) are pluripotent molecules, co‑ordinating cellular functions from early embryonic and postnatal development to tissue repair, regeneration and homeostasis. Etomoxir concentration They are also involved in tumourigenesis, disease progression and the metastasis of various solid tumours. Emerging evidence has indicated that BMPs are able to promote disease progression and metastasis by orchestrating communication between cancer cells and the surrounding microenvironment. The interactions occur between BMPs and epidermal growth factor receptor, hepatocyte growth factor, fibroblast growth factor, vascular endothelial growth factor and extracellular matrix components. Overall, these interactions co‑ordinate the cellular functions of tumour cells and other types of cell in the tumour to promote the growth of the primary tumour, local invasion, angiogenesis and metastasis, and the establishment and survival of cancer cells in the metastatic niche. Therefore, the present study aimed to provide an informative summary of the involvement of BMPs in the tumour microenvironment.The present study aimed to investigate the roles of miR‑132 in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. The myocardial I/R model was established using C57BL/J6 mice. Haematoxylin and eosin staining was performed to observe the injury of myocardial tissues. Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. The in vitro I/R model was established by the hypoxia/reoxygenation method using H9C2 cells. A dual luciferase reporter assay was used to confirm the binding of miR‑132 and sirtuin 1 (SIRT1). Cell pyroptosis was determined using flow cytometry. Reverse transcription‑quantitative PCR was performed to determine the expression of miR‑132, SIRT1 and inflammatory factors. The levels of peroxisome proliferator‑activated receptor gamma coactivator (PGC)‑1α/nuclear factor erythroid‑2‑related factor 2 (Nrf2) signalling, oxidative stress and pyroptosis‑related proteins were detected by western blotting. Apparent histologic injury ahrough activation of PGC‑1α/Nrf2 signalling by targeting SIRT1.Glycoprotein non‑metastatic melanoma protein B (GPNMB) exerts neuroprotective effects on amyotrophic lateral sclerosis and cerebral ischemia reperfusion injury in the central nervous system. However, the expression and function of GPNMB in the peripheral nervous system, particularly following peripheral nerve injury, remains unknown. In the present study, the mRNAs and long non‑coding RNAs of the distal sciatic nerve were profiled via microarray analysis at days 0, 1, 3, 7, 14, 21 and 28 following transection. The results revealed that the expression of GPNMB mRNA was similar to the proliferation tendency of distal acute denervated Schwann cells (SCs), the results of which were further validated by reverse transcription quantitative polymerase chain reaction, western blot analysis and immunohistochemistry. To investigate the function of GPNMB on SCs, recombinant human GPNMB (rhGPNMB) was added to cultured denervated SCs from the distal stumps of transected sciatic nerve. The proliferation, expression and secretion of neurotrophic factors (NTFs) and neural adhesion molecules (NAMs) were subsequently detected. The results demonstrated that GPNMB expression was increased in distal sciatic nerve following transection in vivo, while rhGPNMB promoted the proliferation of SCs as well as expression and secretion of NTFs and NAMs in vitro. Therefore, GPNMB could be a novel strategy for peripheral nerve regeneration.MicroRNA (miR)‑539 has inhibitory effects on certain types of cancer, but its role in pancreatic cancer (PCa) remains unclear. The present study investigated the effects of miR‑539 on PCa, and aimed to determine possible therapeutic targets for the treatment of PCa. The expression of miR‑539 in PCa tissues, paired normal adjacent tissues and PCa cell lines (CAPAN‑2, BxPC3, CFPAC1, SW1990 and PANC1), and human non‑cancerous pancreatic cells (hTRET‑HPNE) was determined and compared. The effects of upregulation and downregulation of miR‑539 on proliferation, apoptosis, cell cycle, invasion, migration and epithelial‑mesenchymal transition (EMT) of PCa cells were investigated. Additionally, the target gene of miR‑539 was predicted and its effects on PCa cells were further investigated. The results revealed low expression of miR‑539 in PCa tissues and cell lines. Additionally, increasing miR‑539 expression inhibited the proliferation, migration, invasion and EMT of PCa cells and induced apoptosis by blocking G1 phase of the cell cycle, while reducing miR‑539 expression had the opposite results. Furthermore, specificity protein 1 (SP1) was found to be the target gene of miR‑539. SP1 promoted the proliferation, migration, invasion and EMT transformation of PCa cells, but these effects were reversed by high expression of miR‑539. Additionally, miR‑539 suppressed the proliferation, metastasis, invasion and EMT transformation of PCa cells through targeting SP1. Therefore, miR‑539 overexpression may contribute toward development of novel therapeutic strategies for PCa in the future.Calbindin‑D28K (Calb1) may protect human lens epithelial cells (HLECs) from apoptosis, which is a process resulting in individual cell death. The protective effects of Calb1 may be attributed to buffering high concentrations of Ca2+. The present study investigated the mechanisms through which Calb1 protects SRA01/04 cells (a human lens epithelial cell line) against apoptosis induced by ultraviolet B (UVB) exposure. Cells transfected with a lentivirus overexpressing Calb1 and control cells were treated with 40 µW/cm2 irradiation for 15 min and then cultured for 24 h. The changes in intracellular Ca2+ were detected by colorimetry, and the protein expression levels of Bad, Bcl‑2 and caspase‑12 were measured by western blot analysis. The intracellular Ca2+ concentration of control HLECs increased significantly following UVB irradiation, whereas in Calb1‑overexpressing cells, the Ca2+ levels remained steady. In the control cells, the expression of Bad and caspase‑12 was upregulated, and that of Bcl‑2 was downregulated.
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