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Objective. To explore the role and mechanism of interleukin-8-mediated autophagy regulation of gastric cancer (GC) cells in GC. Methods. After cell culture, the SGC7901 cell line was separated into the control group and IL-8 (20 ng/mL) group, IL-8 (40 ng/mL) group, and IL-8 (60 ng/mL) group, to verify the effects of the PI3K/Akt signal path on the modulation of autophagy in GC cells. Western blot detected autophagy markers, ATG12-ATG5 complexes, autophagy-associated pathways, and apoptosis-associated factors in GC cells. Transwell was utilized to identify invasion capability. Results. Compared with the control group, the expression of LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 was remarkably elevated in the IL-8 (60 ng/mL) group, IL-8 (20 ng/mL) group, and the IL-8 (40 ng/mL) group. The expression of P62 and Bcl-2 in the IL-8 (60 ng/mL) group was also lower than that of the IL-8 (20 ng/mL) group and IL-8 (40 ng/mL) group, in contrast to the controls. The invasive quantity of GC SGC7901 cells in the IL-8 (60 ng/mL) group was also remarkably higher in contrast to the IL-8 (20 ng/mL) and IL-8 (40 ng/mL) groups. The relative expressions of LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 complex proteins in LY294002 group were considerably elevated. LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 were decreased in the IL-8 + LY294002 group. The relative expressions of P62 and Bcl-2 proteins in the IL-8 + LY294002 group were remarkably elevated, and the invasion of SGC7901 cells in the IL-8 group was elevated. In contrast to the IL-8 group, the invasion quantity of gastric cancer SGC7901 cells in the IL-8 + LY294002 group was considerably decreased. Conclusion. IL-8 promotes autophagy and aggression and suppresses apoptosis of GC SGC7901 cells by regulating PI3K/AKT pathway phosphorylation. [ABSTRACT FROM AUTHOR]

Simple Summary: As one of the most malignant cancers, the mechanisms underlying the occurrence and development of hepatocellular carcinoma (HCC) are complex, and the development of effective treatment strategies has been difficult. Extracellular vesicles (EVs) participate in HCC development in various ways. This review summarizes the latest research on EVs related to Wnt signaling in HCC and expounds on the underlying mechanisms, providing a reference for novel HCC treatment strategies. As the primary type of liver cancer, hepatocellular carcinoma (HCC) causes a large number of deaths every year. Despite extensive research conducted on this disease, the prognosis of HCC remains unclear. Recently, research has largely focused on extracellular vesicles (EVs), and they have been found to participate in various ways in the development of various diseases, including HCC, such as by regulating cell signaling pathways. However, recent studies have reported the mechanisms underlying the regulation of Wnt signaling by EVs in HCC, primarily focusing on the regulation of the canonical pathways. This review summarizes the current literature on the regulation of Wnt signaling by EVs in HCC and their underlying mechanisms. In addition, we also present future research directions in this field. This will deepen the understanding of HCC and provide new ideas for its treatment. [ABSTRACT FROM AUTHOR]

Shenling Baizhu Powder is a traditional Chinese medicine formula that has been used for thousands of years to invigorate spleen, nourish stomach and regulate immune function. The multi-herbal extracts, an improved formular from Shenling Baizhu Powder, were used in our study to investigate its immune-enhancing effects and underling mechanisms. Based on UPLC-Q-TOF-MS and SPME-GC-MS analysis, 106 chemical compounds were identified from the extracts. In vitro assays indicated that the extracts could promote cell proliferation and NO secretion of RAW264.7 cells. RNA-seq and RT-qPCR showed that RAW264.7 cells treated with extracts increased the expression of pro-inflammatory factors IL-1ß, iNOS, TNF-a, and TGF-ß. Western-Blot revealed that the extracts could significantly enhance ERK phosphorylation level, and slightly increased JNK and p38 phosphorylation levels. These data suggest that multi-herbal extracts have a potential of regulating immune response via the JNK/p38/ERK signalling of MAPK pathways in RAW264.7 cells. [ABSTRACT FROM AUTHOR]

The plant architecture of higher plants is regulated through environmental and genetic factors, as well as phytohormones. Phytohormones play a critical role in regulating shoot branching. We determined the branching phenotype of D16 and N99-6, the content of strigolactones, the genetic expression level, and the interaction between auxin and strigolactones. We found that the branching development of the two soybean varieties under shading was significantly slower than that under normal light. The average branch length of N99-6 decreased by 40.9% after shading; however, the branch length of D16 was not significantly affected. Meanwhile, the branch formation rate in D16 was significantly higher than in N99-6. In addition, after shading treatment, the content of strigolactones in D16 and N99-6 axillary buds increased significantly, and the expression of phytochrome genes, PhyA and PhyB, showed opposite changes. However, strigolactone synthesis gene GmMAX4 and signal transduction gene GmMAX2 expression levels of D16 were lower than those of N99-6 after 24 h of shading. In addition, the application of strigolactone inhibitor TIS108 and auxin inhibitor NPA to soybean had no significant effect on the branch phenotype. The expression of the GmMAX2 gene was significantly up-regulated after the external application of the auxin analog, and the expression of auxin transporter gene GmPINI was significantly down-regulated after external application of the strigolactone analog under shade. In this study, we investigated the adverse effect of shade on soybean branching development, which may be due to the interaction of strigolactones with auxins. [ABSTRACT FROM AUTHOR]

Background: In our previous study, we indicated that scutellarin (SCU) induced an anticancer effect in A549 cells. However, whether SCU regulates the radiosensitivity of non‐small cell lung cancer (NSCLC) and its related mechanism is still unclear. Methods: In this study, we explored the anticancer effect induced by iodine‐125 (125I) and SCU at a sensitizing concentration in A549 and H1975 cells. Cellular apoptosis and proliferation were detected by flow cytometry, Bcl‐2/Bax expression level, cell cycle, CCK‐8, and EdU staining. A tumor model using nude mice was also carried out to investigate the combined effect of 125I and SCU in vivo. In addition, the expression level of AKT/mTOR pathway was detected to investigate whether it is linked to the anticancer effect of 125I and SCU. Results: SCU at a sensitizing concentration promoted the 125I‐induced apoptosis and antiproliferative effect in A549 and H1975 cells. Moreover, the same results were obtained in vivo. Based on our findings, the AKT/mTOR pathway was significantly downregulated after combined treatment with 125I and SCU. Conclusions: The results of our study suggested that SCU promotes the anticancer effects induced by 125I in NSCLC cells by downregulating the AKT/mTOR pathway and lays a foundation for future application of this combined treatment. [ABSTRACT FROM AUTHOR]

• AMSP-30 m as a HIF-1α inhibitor relieved the development and severity of rat AIA. • AMSP-30 m showed anti-proliferative and pro-apoptotic effects on AIA synovial cells. • AMSP-30 m exhibited an effective anti-angiogenic effect within AIA rat synovium. • AMSP-30 m inhibited the activation of Shh signaling pathway in AIA rat synovium. Growing evidence indicates that synovial hypoxia-inducible factor 1α (HIF-1α) can be as a promising target for RA therapy. We previously reported that AMSP-30 m as a novel HIF-1α inhibitor had potent activities of anticancer metastasis. This study clarified the therapeutic effects of HIF-1α inhibitor AMSP-30 m on adjuvant-induced arthritis (AIA) in rats and explored the possible mechanisms. AMSP-30 m was given intraperitoneally to AIA rats, and its therapeutic effects and anti-inflammatory activity were evaluated. The influences of AMSP-30 m on synovial apoptosis, angiogenesis and sonic hedgehog (Shh) pathway were examined. We found that, accompanied with the inhibition of synovial HIF-1α expression, AMSP-30 m had potent anti-arthritic and anti-inflammatory effects on AIA rats, evidenced by the reduction in paw swelling, arthritis index, histopathological scores, and the production of IL-1β, IL-6, TNF-α in serum and synovial tissues. AMSP-30 m reduced synovial Ki67 expression and increased TUNEL-positive index, indicating its anti-proliferative and pro-apoptotic effects on AIA synovial cells, which was related to reducing Bcl-2 protein level and increasing Bax, cleaved caspase 3 protein levels. Additionally, AMSP-30 m showed anti-angiogenic effects within AIA synovium, indicated by the reduction of synovial VEGF expression and blood vessels number (especially CD31+/αSMA- immature vessels, but not CD31+/αSMA+ mature vessels). Moreover, AMSP-30 m inhibited the activation of synovial Shh pathway, suggested by the reduction of pathway-related proteins, like Shh, Smo, Gli-1, cyclin D1 and c-Myc. Collectively, HIF-1α inhibitor AMSP-30 m exerted potent anti-arthritic effects on AIA rats possibly by promoting synovial apoptosis, reducing synovial angiogenesis and inhibiting Shh pathway. [ABSTRACT FROM AUTHOR]