Mounting evidences have indicated that terminal differentiation-induced lncRNA (TINCR) contributes to various cellular processes, such as proliferation, apoptosis, autophagy, migration, invasion, and metastasis. However, the function of TINCR in regulating migration of MSCs is largely unknown. In this study, the effects of TINCR on the migration of rat MSCs from the bone marrow were studied by Transwell assays and wound healing assays. Our results suggested that TINCR positively regulated migration of rMSCs. miR-761 mimics suppressed rMSC migration, whereas miR-761 inhibitor promoted migration. Target prediction analysis tools and dual-luciferase reporter gene assay identified Wnt2 as a direct target of miR-761. miR-761 could inhibit the expression of Wnt2. Further, the investigation about the function of TINCR in miR-761-induced migration of rMSCs was completed. These results demonstrated that TINCR took part in the regulation of miR-761-induced migration in rMSCs through the regulation of Wnt2 and its Wnt2 signaling pathway. Taken together, our results demonstrate that lncRNA-TINCR functions as a competitive endogenous RNA (ceRNA) to regulate the migration of rMSCs by sponging miR-761 which modulates the role of Wnt2. These findings provide evidence that lncRNA-TINCR has a chance to serve as a potential target for enhancing MSC homing through the miR-761/Wnt2 signaling pathway.

Purpose. This study was conducted to characterize the expression level of peripheral blood toll-like receptors 9 (TLR9), nuclear factor kappa-B protein 65 (NF-κB p65), and myeloid differentiation factor88 (MyD88) of active systemic lupus erythematosus (SLE) and analyse their clinical significance. Methods. The prospective cohort study enrolled 30 active SLE patients (SG1 group), 30 stable SLE patients (SG2 group), and 20 healthy individuals (RG group) in the First Affiliated Hospital of Hainan Medical University between January 2018 and June 2020. All SLE patients were treated with methylprednisolone tablets. Quantitative polymerase chain reaction (qPCR) was used to determine the levels of TLR9, MyD88, and NF-κB p65 in the peripheral blood mononuclear cell (PBMC). ELISA was adopted for the determination of serum interleukin (IL-6) and tumor necrosis factor-α (TNF-α). Results. Patients in SG1 showed the highest mRNA levels of TLR9, MyD88, and NF-κB p65, followed by SG2, and then RG. SG1 had the highest serum levels of IL-6 and TNF-α, followed by SG2 and RG. The level of TLR9 was positively correlated with the SLE disease activity index (SLEDAI) and negatively correlated with complement component 3 (C3) and complement component 4 (C4). MyD88 and NF-κB p65 were positively correlated with SLEDAI. Conclusion. Compared with a healthy status, SLE induces an increase in TLR9, MyD88, NF-κB p65, IL-6, and TNF-α levels, and the activation of the TLR9-MyD88-NF-κB p65 signal path was associated with the pathogenesis of SLE.

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Highlights Natural compound library screening identified Sanguinarine chloride as a tumor suppressor in SCLC. Sanguinarine chloride exhibits anti-SCLC ability in vitro and in vivo . Sanguinarine chloride upregulates CDKN1A to suppress SCLC development. Sanguinarine chloride enhances the anti-tumor effect of panobinostat in SCLC by promoting cell cycle arrest.

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Objective. To evaluate the clinical efficacy of Gandakang tablets plus methylprednisolone in patients with systemic lupus erythematosus (SLE). Methods. From February 2015 to February 2019, 60 eligible patients with SLE were recruited and assigned via the random number table method at a ratio of 1 : 1 to receive either methylprednisolone (control group) or Gandakang tablets plus methylprednisolone (observation group). The primary endpoint was clinical efficacy, and the secondary endpoints included Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score, immunoglobulin (Ig), inflammatory factor levels, and adverse events. Results. Gandakang tablets plus methylprednisolone were associated with a significantly higher treatment efficacy versus methylprednisolone alone ( P < 0.05 ). Gandakang tablets plus methylprednisolone resulted in significantly lower SLEDAI scores and lower levels of IgG, IgM, IgA, tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), and interleukin-6 (IL-6) versus single medication of methylprednisolone ( P < 0.05 ). The two groups showed a similar incidence of adverse events ( P > 0.05 ). Patients given Gandakang tablets plus methylprednisolone had higher mental health, emotional role, physical role, social functioning, and bodily pain scores versus those receiving the monotherapy of methylprednisolone ( P < 0.05 ). Conclusion. Gandakang tablets plus methylprednisolone is effective in the treatment of SLE by enhancing the patients’ immunity, mitigating the inflammatory response, eliminating negative emotions, and improving their quality of life.