In previous studies oncolytic measles viruses (MVs) have shown significant antitumor activity against various tumors. In our research recombinant MV-Hu191 (rMV-Hu191), established via reverse genetics technology and expressing enhanced green fluorescent protein (EGFP), was evaluated for its therapeutic effects and related mechanisms against nephroblastoma cell lines. We built three different constructs based on rMV-Hu191 to express EGFP effectively. Our experiments showed that rMV-Hu191 expressing EGFP could efficiently infect and replicate in nephroblastoma cell lines. Caspase-induced apoptosis exerted a significant impact on MV-induced cell death, which was accompanied by emission of cellular ATP and high-mobility group protein 1 (HMGB1) and by translocation of calreticulin (CRT). Intratumoral injection of rMV-Hu191-EGFP resulted in significant regression of tumors in a G401 xenograft model. Our results indicate that the MV-Hu191 strain, which is widely used in China, is an appropriate vector for expression of foreign genes and could serve as a potentially good candidate for nephroblastoma therapy mediated by induction of apoptosis-associated immunogenic cell death (ICD).Kinesin family member 2A (KIF2A), a member of the kinesin-13 protein family that functions as a regulator in mitosis, neuron branch extension, etc., is reported to be involved in the pathogenesis of multiple cancers. This study assessed KIF2A effects on cancer cell functions and sensitivity to chemotherapy and its interaction with PI3K/AKT/VEGF signaling when mediating cancer cell functions, and chemosensitivity in non-small cell lung cancer (NSCLC). Human bronchial epithelial cell line BEAS-2B and human NSCLC cell lines NCI-H1299, NCI-H385, NCI-H1650, and A549 were used. The KIF2A and negative control (NC) overexpression plasmids were transfected into A549 cells; KIF2A and NC knock-down plasmids were transfected into NCI-H1299 cells. Rescue experiments were conducted by transfecting PI3K and NC knock-down plasmids into KIF2A overexpression A549 cells and transfecting PI3K and NC overexpression plasmids into KIF2A knock-down NCI-H1299 cells. Proliferation, apoptosis, migration, invasion, CD133+ proportion, sensitivity to chemotherapeutics, and PI3K/AKT/VEGF pathway were assessed. KIF2A mRNA and protein expression levels were elevated in NCI-H1299, NCI-H385, NCI-H1650, and A549 cells compared to BEAS-2B cells. KIF2A overexpression elevated proliferation, migration, invasion, stemness, and resistance to cisplatin but did not affect apoptosis or resistance to pemetrexed in A549 cells. Furthermore, KIF2A knock-down repressed proliferation, migration, invasion, stemness, and resistance to cisplatin, but not to pemetrexed, and it enhanced apoptosis in NCI-H1299 cells. Rescue experiments showed that the PI3K/AKT/VEGF pathway compensated for KIF2A effects on cell functions and sensitivity to cisplatin in A549 and NCI-H1299 cells. In conclusion, KIF2A advocates NSCLC cell viability, mobility, stemness, and chemoresistance to cisplatin by activating the PI3K/AKT/VEGF signaling pathway.Gynecologic cancer is a serious global healthcare issue with high rates of mortality and morbidity. In recent years, tumor immunity and immunotherapy have attracted extensive attention for treatment of gynecological cancers. Indoleamine 2, 3-dioxygenase 1 (IDO1) plays a critical role in cancer immune escape, and its inhibition has been explored for immune-targeted therapies for many malignancies. However, knowledge about IDO1 involvement in the pathogenesis of gynecological cancers and its therapeutic potential is still evolving. In the current study, we integrated bioinformatics analysis of the prognostic value and immune function of IDO1 in gynecologic malignancies using Oncomine, GEPIA, HPA, TIMER, TISIDB, SurvExpress and Metascape database. Comprehensive analysis revealed that the transcription levels of IDO1 were significantly overexpressed in patients with gynecologic cancers, and IDO1-co-expressed gene signatures may be useful potential prognostic markers for gynecologic cancers. Furthermore, increased IDO1 expression correlated with immune infiltration cells, immune marker sets, and immunomodulators in gynecological cancers. These findings suggest that IDO1 plays an important role in immune infiltration and could potentially be an immunotherapeutic target for gynecological cancers. However, future large-scale and comprehensive research is required to validate our results.EGb 761 has some protective effects on AD and can improve the cognitive functions of AD mice. However, the underlying molecular mechanisms are unknown. Here, we investigated the function of bilobalide, the effective component of EGb 761, in neuroinflammation and autophagy during AD. LPS-treated BV-2 cells were used as an in vitro model for neuroinflammation. The APP/PS1 AD mouse line was used to examine the function of bilobalide in AD. ELISA and qRT-PCR were used to measure the levels of proinflammatory cytokines, including TNF-α, IL-6 and IL-1β. Western blotting was employed to determine the protein levels of p-p65, iNOS, COX-2, LC3, beclin-1, p62 and p-STAT3. Immunostaining was applied to examine the number of autophagosomes. LPS treatment induced inflammatory responses and inhibited autophagy in BV-2 cells. Bilobalide suppressed LPS-induced neuroinflammation and promoted autophagy. Furthermore, bilobalide treatment increased the lincRNA-p21 levels, which suppressed STAT3 signalling. Knockdown of lincRNA-p21 reversed the effects of bilobalide. Overexpression of lincRNA-p21 promoted autophagy and inhibited neuroinflammation as well while STAT3 inhibitor blocked the effects of si-lincRNA-p21.  https://www.selleckchem.com/products/gsk2830371.html  In vivo experiments revealed that bilobalide improved the learning and memory capabilities of APP/PS1 AD mice. Bilobalide improves the cognitive functions of APP/PS1 AD mice. Mechanistically, bilobalide suppresses inflammatory responses and promotes autophagy possibly by upregulating lincRNA-p21 levels.Apigenin (APG), a natural flavonoid with anti-inflammatory and anti-fibrosis properties, has been shown to play a protective role in diabetic nephropathy (DN), but their molecular protection mechanism for miRNA has not been elucidated in detail. This study was designed to focus on exploring its protective role in DN and whether miR-423-5p-upstream stimulating factor 2 (USF2) axis was involved in its protective mechanism. The in vivo model of rat was induced by streptozotocin (STZ) and the in vitro model of renal tubular epithelial cell (RTEC) was induced by high glucose (HG). Our in vivo study revealed that APG had different protective effects on inflammation, renal fibrosis and epithelial mesenchymal transition (EMT) in DN rats, which is mainly reflected in that the inflammatory factors (IL-6, IFN-γ, TNF-α) were obviously down-regulated, the renal fibrosis markers (IV-C, FN, Col I) were significantly inhibited, the E-cadherin (EMT factors) was significantly up-regulated, while the vimentin and α-SMA (EMT factors) were significantly down-regulated, and the renal function indexes (serum Cr, BUN) were significantly improved.