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01) and were associated with tumor development in patients. Gain‑ and loss‑of‑function experiments highlighted the function of NRP1 in promoting EC proliferation, motility and capillary‑like tube formation and in reducing apoptosis. NRP1 overexpression led to significantly decreased EC markers (PECAM‑1, angiogenin, PIGF and MMP‑9) expression levels and reduced the vascular maturity. MAPK7, TPM1, RRBP1, PTPRK, HSP90A, PRKD2, PFKFB3, RGS4 and SPARC were revealed to play important roles in this process. SEMA4D was revealed to be a key protein associated with NRP1 in ECs. These data indicated that NRP1‑promoted angiogenesis may be induced at the cost of reducing maturity of the ECs. NRP1 may also be a therapeutic target for antiangiogenic strategies and a candidate prognostic marker for tumors.The impacts of post‑operative abdominal infectious complications increase hematogenous distant metastasis and result in poor long‑term survival after curative resection. Even if curative resection can be performed, the presence of circulating tumor cells is affected. The liver, the most common site of metastases, is an important organ in innate immune surveillance. However, the molecular mechanisms of distant hematogenous metastasis are not yet fully known. Platelets are crucial components in the tumor microenvironment that function to promote tumor progression and metastasis. The purpose of this study was to identify the effect of platelets on escape from innate immune surveillance in post‑operative abdominal infectious complications. Platelet adherence was assessed by co‑culturing human pancreatic cancer cells including transforming growth factor (TGF‑β)‑treated BxPC‑3. CD44 isoform, transcription factors and epithelial‑mesenchymal transition markers were examined using western blotting. We also assessed whmune surveillance by becoming surrounded by adhered activated platelets. Therefore, it may be necessary to administer antiplatelet agents to prevent distant hematogenous metastasis when post‑operative abdominal infectious complications occur.The present study aimed to examine the effects of FcγRIIB on systemic lupus erythematosus (SLE) and to investigate the underlying mechanisms. For this purpose, lentiviral vector carrying the membrane‑bound type FcγRIIB gene (mFcγRIIB lentivirus) and soluble FcγRIIB (sFcγRIIB) protein were used to treat B cells from patients with SLE. The B cells were treated with calf thymus DNA (ctDNA) and anti‑calf thymus DNA‑immune complexes (anti‑ctDNA‑IC). mFcγRIIB lentivirus and sFcγRIIB protein were also injected into MRL/lpr SLE mice. The results revealed that anti‑ctDNA‑IC treatment significantly downregulated the IgG antibody secretion of B cells treated with mFcγRIIB lentivirus. mFcγRIIB and sFcγRIIB decreased the phosphorylation level of Bruton's tyrosine kinase (BTK) in B cells, and increased the phosphorylation level of Lyn proto‑oncogene (Lyn), docking protein 1 (DOK1) and inositol polyphosphate‑5‑phosphatase D (SHIP). mFcγRIIB promoted the apoptosis of B cells. Following the treatment of MRL/lpr SLE mice with for the prevention and treatment of SLE.Chemoresistance to platinum‑based chemotherapy for ovarian cancer in the advanced stage remains a formidable concern clinically. Increasing evidence has revealed that apoptosis represents the terminal events of the anti‑tumor mechanisms of a number of chemical drugs and has a close association with chemoresistance in ovarian cancer. The B‑cell lymphoma‑2 (Bcl‑2) family plays a crucial role in apoptosis and has a close association with chemoresistance in ovarian cancer. Some drugs that target Bcl‑2 family members have shown efficacy in overcoming the chemoresistance of ovarian cancer. A BH3 profiling assay was found to be able to predict how primed a cell is when treated with antitumor drugs. The present review summarizes the role of the Bcl‑2 family in mediating cell death in response to antitumor drugs and novel drugs that target Bcl‑2 family members. The application of the new functional assay, BH3 profiling, is also discussed herein. Furthermore, the present review presents the hypothesis that targeting Bcl‑2 family members may prove to be helpful for the individualized therapy of ovarian cancer in clinical practice and in laboratory research.Icariside II (ICS II) has been reported to have protective effects against oxidative stress. However, whether ICS II protects cardiomyocytes from myocardial infarction (MI), and the associated underlying mechanisms, remain to be elucidated. Therefore, the current study investigated the effects of ICS II on hypoxia‑injured H9c2 cells, as well as the associated molecular mechanisms. A hypoxic injury model was established to emulate the effects of MI. The effects of ICS II on the proliferation of rat cardiomyocyte H9c2 cells were assessed with cell counting kit‑8 assays. The apoptotic status of the cells was assessed by flow cytometry, and the expression of apoptosis‑related proteins was analyzed by western blotting. A microRNA (miRNA/miR) microarray was used to quantify the differential expression of miRNAs after ICS II treatment, and the levels of miR‑7‑5p were further quantified by reverse transcription‑quantitative PCR. Whether ICS II affected hypoxia‑injured cells via miR‑7‑5p was subsequently examined, and the target of miR‑7‑5p was also investigated by bioinformatics analysis and luciferase reporter assays. The effects of ICS II on the PI3K/Akt pathway were then evaluated by western blot analysis. Hypoxia treatment decreased viability and the migration and invasion abilities of H9c2 cells, and also induced apoptosis. ICS II significantly increased viability and reduced hypoxia‑associated apoptosis. Moreover, ICS II treatment led to the upregulation of miR‑7‑5p, and the protective effects of ICS II were found to rely on miR‑7‑5p. [https://www.selleckchem.com/products/tno155.html click here] Moreover, BTG anti‑proliferation factor (BTG2) was identified as a direct target of miR‑7‑5p, and overexpression of BTG2 inhibited the protective effects of miR‑7‑5p. Finally, ICS II treatment resulted in the activation of the PI3K/Akt signaling pathway, which is essential for the survival of H9c2 cells under hypoxic conditions. In summary, ICS II reduces hypoxic injury in H9c2 cells via the miR‑7‑5p/BTG2 axis and activation of the PI3K/Akt signaling pathway.