Isolated compounds from Sargassum thunbergii (S. thunbergii) have shown to exhibit diverse biological activities, including anti-cancer activity. In this study, we examined the effect of sulfated galactofucan (SWZ-4-H), which was successfully isolated from S. thunbergii, and its underlying mechanism on human lung cancer (LC) A549 cell growth in vitro and in vivo. In vitro experiment indicated that SWZ-4-H decreased cell growth and number in a dose-dependent manner (P < 0.05 vs. control). Besides, cells treated with SWZ-4-H had irregular morphology, including increased cell volumes, and large nuclei, which suggested senescence-like changes. Moreover, SWZ-4-H increased senescence-related β-galactosidase (SA-β-Gal) staining in a dose-dependent manner; however, while lower (1 mg mL⁻¹) concentration induced mainly senescence without causing cell death, higher dosage (3 mg mL⁻¹) induced both senescence and cell death. The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner. Moreover, in vivo experiment showed that SWZ-4-H significantly reduced the tumor volume without affecting the body weight. To sum up, our data indicated that SWZ-4-H could induce lung cancer senescence by regulating p53, p21, p16, and p-Rb, thus providing a novel perspective on anti-cancer mechanisms of SWZ-4-H in human lung cancer A549 cells.

The disordered expression of ZNF143 is closely related to the malignant progression of tumours. However, the basic control mechanism of ZNF143 in glioma has not yet been clarified. Therefore, we tried to find a new pathway to illustrate the function of ZNF143 in glioma. To explore the function of KPNA2 in the development of glioma, we used survival analysis by the Kaplan‒Meier method to assess the overall survival (OS) of patients with low and high KPNA2 expression in the TCGA and CGGA cohorts. Western blotting assays and RT‒PCR assays were utilized to determine the expression level of KPNA2 in glioma cells. The interaction between ZNF143 and KPNA2 was confirmed by ChIP assays. Proliferation was assessed by CCK-8 assays, and migration was evaluated by wound healing and Transwell assays. Apoptosis was determined by flow cytometry, and the expression level of YAP/TAZ was visualized using an immunofluorescence assay. The expression levels of LATS1, LATS2, YAP1, and p-YAP1 were determined. Patients with low KPNA2 expression showed a better prognosis than those with high KPNA2 expression. KPNA2 was found to be upregulated in human glioma cells. ZNF143 can bind to the promoter region of KPNA2. Downregulation of ZNF143 and KPNA2 can activate the Hippo signalling pathway and reduce YAP/TAZ expression in human glioma cells, thus inducing apoptosis of human glioma cells and weakening their proliferation, migration and invasion. In conclusion, ZNF143 mediates the Hippo/YAP signalling pathway and inhibits the growth and migration of glioma cells by regulating KPNA2.

Osteoporosis (OP) is a systemic bone degenerative disease characterized by low bone mass and deteriorated microarchitecture of bone tissue, causing high morbidity and mortality rates. Bone resorption by overactivated osteoclasts (OCs) is the main cause of osteoporosis. Glucuronomannan and its oligomers (Gs) and their sulfated derivatives (SGs) were previously prepared. The anti-osteoporosis activities of these glycans were evaluated. Firstly, we determined the viability of RAW264.7 by CCK-8 test. Nextly, we investigated the inhibitory effects of Gs and SGs on the differentiation of RAW264.7 cells into OCs using tartrate-resistant acid phosphatase (TRAP) staining, F-actin ring staining, qualitative reverse-transcription polymerase chain reaction(qRT-PCR) and western blotting. TRAP staining revealed that Gs significantly blocked RANKL-induced OC generation while SGs did not exhibit this ability. F-actin staining assays demonstrated that Gs inhibits RANKL-induced actin ring formation. qRT-PCR analyses indicated that Gs dose-dependently inhibited the expression of OCs marker genes including Trap, NFATc1, c-Fos, DC-Stamp and ATP60 during the differentiation process, while SGs did not suppress. Regarding the mechanism of Gs, it was found that Gs suppressed osteoclastogenesis via inhibiting the degradation of IRF-8 and interfering with NF-κB pathway activation. Together, these results suggest that Gs have the ability to inhibit osteoclastogenesis by modulating IRF-8 signaling.

Postmenopausal osteoporosis (PMO) is a prevalent metabolic bone disease with high morbidity and serious complications. Here, we studied the effect of glycyrrhizin on bone metabolism using the ovari... 目的：绝经后骨质疏松症（PMO）是一种常见的代谢性骨病, 发病率高, 并发症严重。本研究应用去卵巢（OVX）小鼠模型研究了甘草酸苷对骨代谢的影响。方法：通过实时定量聚合酶链反应和骨吸收实验, 评估RAW264.7细胞和骨髓单核细胞（BMMs）中破骨细胞相关基因的表达和破骨功能。动物实验选用雌性C57BL/6J小鼠, 随机分为假手术组、去势组和去势+甘草酸苷组。通过显微计算机断层扫描、双X射线...