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Lupus nephritis (LN) is a kidney disorder that is a critical cause of mortality in patients with systemic lupus erythematosus. The present study aimed to explore the protective role of complement component 1q (C1q) on LN and the underlying mechanism involving the nuclear factor (NF)‑κB singling pathway. MRL/lpr mice served as the LN mouse model, and pcDNA‑C1q was injected into LN mice to determine the role of C1q. C1q mRNA expression was detected using reverse transcription‑quantitative PCR. Urine protein and blood urea nitrogen (BUN) levels were measured, and the histological damage index was determined using H&amp;E staining. ELISA was used to measure the levels of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑1β, IL‑6, anti‑C1q and anti‑double stranded DNA (dsDNA). CD68‑ and Ki67‑positivity were detected using immunofluorescence, and NF‑κB‑related protein expression was examined using western blotting. C1q mRNA expression was downregulated in renal tissues of LN mice. Overexpression of C1q decreased urine protein, BUN levels and the histological damage index in LN mice. The levels of TNF‑α, IL‑1β, IL‑6, anti‑C1q and anti‑dsDNA in renal tissues of LN mice were also reduced after pcDNA‑C1q treatment. Additionally, overexpression of C1q decreased the CD68‑ and Ki67‑positivity in glomeruli and attenuated the expression of NF‑κB‑related proteins. Phorbol 12‑myristate 13‑acetate, an NF‑κB pathway activator, reversed the inhibitory effect of C1q on inflammation, macrophage infiltration and mesangial cell (MC) proliferation in renal tissues of LN mice. Thus, it was demonstrated that C1q ameliorated inflammation and macrophage infiltration and decreased MC proliferation in renal tissues of LN mice by inhibiting the NF-κB pathway.The present study explored whether bone morphogenetic proteins (BMPs) and Wnt/β‑catenin signaling pathways were involved in the 1,25(OH)2D3‑induced inhibition of osteogenic differentiation in bone marrow‑derived mesenchymal stem cells (BMSCs). To evaluate the osteogenic differentiation of BMSCs, the expression levels of ossification markers, including BMP2, Runt‑related transcription factor 2 (Runx2), Msh homeobox 2 (Msx2), osteopontin (OPN) and osteocalcin (OCN), and the activity of alkaline phosphatase (ALP), as well as the calcified area observed by Alizarin red‑S staining, were investigated. Chromatin immunoprecipitation (ChIP) assay was used to detect the effect of 1,25(OH)2D3 on the DNA methylation and histone modification of BMP2, while an immunoprecipitation (IP) assay was performed to assess the crosstalk between Smad1 and disheveled‑1 (Dvl‑1) proteins. It was observed that 1,25(OH)2D3 significantly decreased the expression levels of BMP2, Runx2, Msx2, OPN and OCN, and reduced ALP activity and the calcified area in BMSCs, whereas these effects were rescued by BMP2 overexpression. ChIP assay revealed that BMSCs treated with 1,25(OH)2D3 exhibited a significant increase in H3K9me2 level and a decrease in the acetylation of histone H3 at the same BMP2 promoter region. In addition, 1,25(OH)2D3 treatment promoted the nuclear accumulation of β‑catenin by downregulating BMP2. Furthermore, the β‑catenin signaling inhibitor XAV‑939 weakened the inhibitory effect of 1,25(OH)2D3 on osteogenic differentiation. Additionally, knockdown of β‑catenin rescued the attenuation in Dvl‑1 and Smad1 interaction caused by 1,25(OH)2D3. Overexpression of Smad1 also reversed the inhibitory effect of 1,25(OH)2D3 on osteogenic differentiation. Taken together, the current study demonstrated that 1,25(OH)2D3 inhibited the differentiation of BMSCs into osteoblast‑like cells by inactivating BMP2 and activating Wnt/β‑catenin signaling.Multiple endocrine neoplasia type 1 (MEN1) is a rare genetic disorder that is inherited in an autosomal dominant manner. The characteristics of the disease are the combined occurrence of tumors in glands of the endocrine system, such as the parathyroid glands, pituitary gland and endocrine pancreas. Germline mutations in the MEN1 gene are associated with the occurrence of MEN1 and genetic testing for this gene is generally used as a basis for diagnosis. In this paper, a case of MEN1 in a middle‑aged Japanese woman is reported. Direct sequencing analysis of the patient's DNA was performed and it revealed a MEN1 gene heterozygous germline (NM_130799.2c.930delG) mutation in exon 5. [https://www.selleckchem.com/products/PD-98059.html click here] This deletion/frameshift mutation produced a stop codon in the downstream sequence (NP_570711.1p.Glu273LysfsTer7). To the best of our knowledge, this is the first report describing the NM_130799.2c.930delG mutation as the basis for MEN1.Breast cancer (BC) is the most frequently diagnosed type of cancer, and the leading cause of cancer‑associated mortality in females worldwide. The aim of the present study was to investigate the prognostic and therapeutic potential of NUF2 in BC. The expression levels of NUF2 in BC tissues and cell lines were evaluated via bioinformatics, reverse transcription‑quantitative PCR, western blot analysis and immunohistochemistry (IHC). In addition, the effect of NUF2 knockdown on BC cell proliferation and apoptosis was investigated using small interfering RNA (siRNA) technology. Bioinformatics and IHC analysis showed that NUF2 was overexpressed in BC tissues. Furthermore, western blot and RT‑qPCR analyses demonstrated that NUF2 was upregulated in BC cells. In addition, BC cells transfected with NUF2 siRNA exhibited significantly decreased proliferation and colony formation, and increased apoptosis, compared with the control. Additionally, cell cycle analysis revealed that NUF2 induced G0/G1 cell cycle arrest by inhibiting cyclin B1 expression. Collectively, the present study suggested that NUF2 may represent a promising prognostic biomarker and a potential therapeutic target for BC.Ankylosis progressive homolog (ANKH) is associated with fibroblast ossification in ankylosing spondylitis (AS). As the human ANKH gene is poorly characterized relative to its murine counterpart, the aim of the present study was to examine ANKH expression in ligament tissue isolated from patients with AS and the role played by this gene in AS‑associated fibroblast ossification. Fibroblasts were isolated from ligament tissue collected from patients with AS and ligament tissue from individuals with spinal cord fractures, then cultured. Fibroblasts from patients with AS were subsequently transfected with an ANKH overexpression vector, while those collected from individuals with spinal cord fractures were transfected with small interfering RNA specific for ANKH. Cell viability, apoptosis and mineralization were analyzed using MTT assays, flow cytometry and Alizarin Red staining, respectively. Furthermore, ANKH mRNA and protein expression levels were analyzed using reverse transcription‑quantitative PCR and western blotting analysis, respectively.