scholarly journals Effects of Inonotus obliquus Polysaccharides on Proliferation, Invasion, Migration, and Apoptosis of Osteosarcoma Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Baohui Su ◽  
Xuezhi Yan ◽  
Yuezhong Li ◽  
Junshan Zhang ◽  
Xiaoyan Xia
Keyword(s):  
Signaling Pathway ◽  
Migration And Invasion ◽  
Control Group ◽  
Osteosarcoma Cells ◽  
Inonotus Obliquus ◽  
U2os Cells ◽  
Inonotus Obliquus Polysaccharide ◽  
Related Proteins ◽  
Experimental Group

Objectives. To observe the effect of Inonotus obliquus polysaccharide (IOP) on the proliferation, invasion, migration, and apoptosis of osteosarcoma cells and to elucidate its underlying molecular mechanism. Methods. IOP was extracted from Inonotus obliquus, human osteosarcoma MG-63 cells and U2OS cells were cultured in vitro, and the effects of IOP on the proliferation, migration, invasion, and apoptosis of MG-63 cells and U2OS cells were determined by CCK-8 assays, cell scratch assays, transwell assays, and flow cytometry, respectively. Western blot was used to detect the expression of related proteins in the Akt/mTOR and NF-κB signaling pathways. Results. Compared with the control group, MG-63 cells and U2OS cells treated with IOP of 80 μg/ml, 160 μg/ml, and 320 μ g/ml in the experimental group had significantly lower proliferation activity, decreased migration and invasion ability, and increased apoptosis rate ( P < 0.05 ). Furthermore, IOP could significantly inhibit the activation of the Akt/mTOR and NF-κB signaling pathway ( P < 0.05 ). Conclusion. IOP can regulate the proliferation, migration, invasion, and apoptosis of osteosarcoma cells by inhibiting the activation of the Akt/mTOR signaling pathway. It has antitumor activity on osteosarcoma and has the potential of clinical application in osteosarcoma treatment.

scholarly journals Propofol affects the biological behavior of ovarian cancer SKOV3 cells via ERK1/2-MMP-2/9 signaling pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 233-238
Author(s):  
Ruchang Yin ◽  
Chunyan Zhang ◽  
Aizhi Gen ◽  
Yanxiao Li ◽  
Hailei Yang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
New Drugs ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Control Group ◽  
High Dose ◽  
Fat Emulsion ◽  
Skov3 Cells

Purpose: To investigate the effect of propofol on the biological behavior of ovarian cancer SKOV3 cells, and the mechanism of action involved. Methods: SKOV3 cells cultured in vitro were randomly divided into control group, fat emulsion group, low-dose propofol group (LDPG, 25 μmol/L), medium-dose propofol group (MDPG) (50 μmol/L) and high-dose propofol group (HDPG) (100 μmol/L). Apoptosis was determined by flow cytometry, while Transwell assay was used to measure the migration and invasion abilities of the cells. The protein levels of ERK1/2, MMP-2, MMP-9 were assayed with Western blotting. Moreover, the cells were transfected with siERK, and the regulatory effect of propofol on ERK1/2-MMP-2/9 signaling pathway was determined. Results: Apoptosis in HDPG was significantly reduced, relative to MDPG, while migration and invasion were enhanced, relative to MDPG (p < 0.05). Moreover, MMP-2, ERK1/2, and MMP-9 proteins were significantly higher in MDPG and HDPG than in control, fat emulsion and LDPGs (p < 0.05), and were upregulated in HDPGs, relative to MDPG (p < 0.05). In contrast, propofol did not up-regulate these proteins in siRNA-treated cells. Conclusion: Propofol enhances the migration, proliferation, and invasive ability SKOV3 cells, and upregulates the expressions of MMP-2, ERK1/2, and MMP-9 in these cells, via a mechanism related to the activation of ERK1/2-MMP-2/9 signaling route. These properties provide novel leads for the development of new drugs for ovarian cancer Keywords: Propofol, ERK1/2-MMP-2/9 signal route, Ovarian cancer, Biological behavior

Effects and Mechanisms of Tripartite Motif Containing 14 Downregulation on Proliferation, Migration, and Invasion of Cancerous Pancreatic PANC-1 Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 402-406
Author(s):  
Huaping Gong ◽  
Long Chen ◽  
Ruipeng Dong
Keyword(s):  
Protein Expression ◽  
Signaling Pathway ◽  
Cellular Proliferation ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Sirna Transfection ◽  
Akt Phosphorylation

This study aimed to investigate the effect and mechanism of TRIM14 downregulation on the apoptosis, migration, and invasion of cancerous pancreatic PANC-1 cells. PANC-1 cells cultured in vitrowere classified to a control (normal culture), negative (neutral siRNA transfection), and siTRIM14 group (TRIM14 siRNA transfection). RT-PCR was adopted to test TRIM14 mRNA expression. Cellular proliferation was determined by CCK-8, and transwell chamber invasion and apoptosis by flow cytometry. AKT signaling pathway related proteins CyclinD1, MMP-2, Bcl-2, and AKT phosphorylation, and TRIMI14 protein expression, were determined by western blotting. Compared with the control group, TRIMI14 expression, cellular proliferation ability, infiltration, transfer AKT phosphorylation, and TRIMI14, CyclinD1, MMP-2, and Bcl-2 protein expression were greatly reduced in siTRIM14 cells, and the apoptotic ability was significantly enhanced (P < 0.05). However, no striking differences were detected between the negative and control groups (P > 0.05). Downregulating TRIM14 expression can inhibit the proliferation, invasion, and migration of PANC-1 cells, and promote apoptosis. The mechanism may be associated with the inhibition of AKT signaling pathway activation.

scholarly journals IL-38 restrains inflammatory response of collagen-induced arthritis in rats via SIRT1/HIF-1α signaling pathway

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Bing Pei ◽  
Keyan Chen ◽  
Shenglai Zhou ◽  
Dongyu Min ◽  
Weiguo Xiao
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Joint Damage ◽  
Inhibitory Effect ◽  
Angiogenic Factor ◽  
Inflammatory Factors ◽  
Control Group ◽  
Collagen Induced Arthritis ◽  
Related Proteins

Abstract Objective: To observe the restraining effect of IL-38 on inflammatory response in collagen-induced arthritis rats (CIA), and to explore the regulatory mechanism of SIRT1/HIF-1α signaling pathway. Methods: 40 SD rats were randomly divided into Control group, CIA group, CLL group and CLH group, with 10 rats in each group; CIA rat model was established. The effects of IL-38 on arthritis index, inflammatory response, osteogenic factor and angiogenic factor were observed by methods including HE staining, ELISA, immunohistochemical and immunofluorescence. Human synoviocytes were cultured in vitro, and SIRT1 inhibitors were added to detect the expression for relating factors of SIRT1/HIF-1α signaling pathway by Western blot. Results: IL-38 could alleviate CIA joint damage and restrain inflammatory response, could up-regulate the expression of OPG in CIA rats and could down-regulate the expression of RANKL and RANK. IL-38 could restrain the expression of VEGF, VEGFR1, VEGFR2 and HIF. Moreover, we found that IL-38 could up-regulate the SIRT1 expression and down-regulate the HIF-1α, TLR4 and NF-KB p65 expression in CLL and CLH groups. From the treatment of synoviocytes to simulate the CIA model and the treatment of SIRT1 inhibitors, we demonstrated that the inhibitory effect of IL-38 on inflammatory factors and regulation of SIRT1/HIF-1α signaling pathway-related proteins were inhibited. Conclusion: IL-38 can restrain the inflammatory response of CIA rats, can promote the expression of osteogenic factors, can inhibit neovascularization, and can alleviate joint damage in rats. The mechanism may be related to the regulation of SIRT1/HIF-1α signaling pathway.

scholarly journals Inhibitory Effects of Inonotus obliquus Polysaccharide on Inflammatory Response in Toxoplasma gondii-Infected RAW264.7 Macrophages

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Kexin Yan ◽  
Hongyuan Zhou ◽  
Meng Wang ◽  
Haitao Li ◽  
Rui Sang ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Protective Effects ◽  
Inonotus Obliquus ◽  
Monocyte Chemoattractant Protein 1 ◽  
Raw264.7 Macrophages ◽  
Inonotus Obliquus Polysaccharide

Our previous reports have shown that Inonotus obliquus polysaccharide (IOP) has protective effects against Toxoplasma gondii (T. gondii) infection in vivo. The aim of the present research is to explore the in vitro anti-inflammatory effects of IOP and its mechanism in RAW264.7 macrophages infected by T. gondii. In this study, it is indicated that IOP decreased the excessive secretion of inflammatory cytokines tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-4, and IL-6 in T. gondii-infected RAW264.7 macrophages. IOP effectively suppressed the mRNA expression of these cytokines and chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α). Moreover, IOP inhibited the phosphorylation of inhibitor kappa B kinase α/β (IKKα/β), inhibitor κBα (IκBα), p65 in nuclear factor-kappa B (NF-κB) signaling pathway and p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK1/2) in mitogen-activated protein kinases (MAPKs) signaling pathway. Meantime, IOP prevented NF-κB p65 and c-Jun translocation from the cytoplasm to the nucleus. Further, IOP downregulated the protein expression of toll-like receptor 2 (TLR2) and TLR4 in T. gondii-infected RAW264.7 macrophages. The above results suggest that IOP can inhibit the inflammatory response infected with T. gondii via regulating TLR2/TLR4-NF-κB/MAPKs pathways and exerting its anti-T. gondii role in vitro.

scholarly journals CORO1C is Associated With Poor Prognosis and Promotes Metastasis Through PI3K/AKT Pathway in Colorectal Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Zongxia Wang ◽  
Lizhou Jia ◽  
Yushu sun ◽  
Chunli Li ◽  
Lingli Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Poor Prognosis ◽  
Akt Signaling ◽  
Actin Binding ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Related Proteins

Trophoblast cell surface protein 2 (Trop2) is one of the cancer-related proteins that plays a vital role in biological aggressiveness and poor prognosis of colorectal cancer (CRC). The study of the Trop2 related network is helpful for us to understand the mechanism of tumorigenesis. However, the effects of the related proteins interacting with Trop2 in CRC remain unclear. Here, we found that coronin-like actin-binding protein 1C (CORO1C) could interact with Trop2 and the expression of CORO1C in CRC tissues was higher than that in paracarcinoma tissues. The expression of CORO1C was associated with histological type, lymph node metastasis, distant metastasis, AJCC stage, venous invasion, and perineural invasion. The correlation between CORO1C expression and clinical characteristics was analyzed demonstrating that high CORO1C expression in CRC patients were associated with poor prognosis. Furthermore, CORO1C knockdown could decrease the cell proliferation, colony formation, migration and invasion in vitro and tumor growth in vivo. The underlying mechanisms were predicted by bioinformatics analysis and verified by Western blotting. We found that PI3K/AKT signaling pathway was significantly inhibited by CORO1C knockdown and the tuomr-promoting role of CORO1C was leastwise partly mediated by PI3K/AKT signaling pathway. Thus, CORO1C may be a valuable prognostic biomarker and drug target in CRC patients.

scholarly journals GLS1 Promotes The Malignant Progression of Osteosarcoma

2021 ◽  
Author(s):  
ZENG TONG ◽  
Peng Lei ◽  
YIN JUNQIANG ◽  
LIU WEIHAI ◽  
ZHANG DI ◽  
...  
Keyword(s):  
Protein Expression ◽  
Western Blot ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Metabolic Reprogramming ◽  
Migration And Invasion ◽  
Osteosarcoma Cells ◽  
U2os Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Osteosarcoma (OS) is the most frequent and high-grade young malignant bone tumor. The prognosis is still poor despite the use of combined therapy involving maximal surgical resection, radiotherapy and chemotherapy. Metabolic reprogramming currently is recognized as one of the hallmarks of cancer. Glutaminase 1(GLS1) has been associated with progression of tumor cell through CDK4 signaling pathway.Methods: In the study, Western blot was used to detect the expression of GLS1 protein in tumor and adjacent normal tissues of osteosarcoma patients, and Western blot was used to detect the expression of GLS1 protein in osteosarcoma cell lines. GLS1 siRNA was transfected into osteosarcoma U2OS cells. Western blot was used to detect the expression of GLS1 protein. MTT and clone formation assay were used to detect cell proliferation. Transwell chamber assay was used to detect migration and invasion. Western blot was used to detect the expression of CDK4 protein in GLS1 knockdown U2OS cells. CB-839 was used to treat U2OS cells. The IC50 value of CB-839 was detected by MTT. The proliferation and migration of CB-839 were detected by clone formation, scratch test, RNA seq sequencing, q-PCR and Western blot.Results: (1) GLS1 was highly expressed in osteosarcoma tissues and cell lines; (2) After transfection, compared with the control group, GLS1 protein expression and CDK4 protein expression of U2OS cells in the knockdown group were significantly down regulated. In vitro experiments showed that the proliferation, migration and invasion of U2OS cells were significantly down regulated; (3) CB-839 promoted apoptosis and inhibited the proliferation and migration of osteosarcoma cells by acting on upstream transcription factors EGR1 and FOXO1. Conclusion: GLS1 can promote the proliferation, migration and invasion of osteosarcoma cells by affecting the cell cycle of CDK4 signaling pathway, and can be used as a potential prognostic indicator and therapeutic target for osteosarcoma patients.

scholarly journals Has-miR-875-5p Inhibits Tumorigenesis By Targeting USF2 Via TGF-β Signaling Pathway in Gastric Cancer

2021 ◽  
Author(s):  
Shenshuo Gao ◽  
Zhikai Zhang ◽  
Xubin Wang ◽  
Yan Ma ◽  
Chensheng Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Research Direction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
New Research ◽  
Related Proteins

Abstract Background: Gastric cancer (GC) is one of the most common malignancies, and more and more evdiences show that the pathogenesis is regulated by various miRNAs. In this study, we investigated the role of miR-875 in GC. Methods: The expression of miR-875-5p was detected in human GC specimens and cell lines by miRNA RT-PCR. The effect of miR-875-5p on GC proliferation was determined by CCK-8 proliferation assay and EDU assay. Migration and invasion were examined by transwell migration and invasion assay and wound healing assay. The interaction between miR-875-5p and its target gene USF2 was verified by a dual luciferase reporter assay. The effects of miR-875-5p in vivo were studied in xenograft nude mice models. Related proteins were detected by Western blot. Results: The results showed that miR-875-5p inhibited the proliferation, migration and invasion of gastric cancer cells in vitro, and inhibited tumorigenesis in vivo. USF2 proved to be a direct target of miR-875-5p. Knockdown of USF2 partially counteracts the effects of miR-875-5p inhibitors. Overexpression of miR-875-5p can inhibit proliferation, migration, and invasion through the TGF-β signaling pathway by down-regulation of USF2 in GC, providing a new research direction for the diagnosis and targeted therapy of GC.Conclusions: MiR-875-5p can inhibited the progression of GC by directly targeting USF2 and negatively regulating TGF-β signaling pathway. In the future, miR-875-5p is expected to be used as a potential therapeutic target for GC therapy.

scholarly journals Cordycepin augments the chemosensitivity of osteosarcoma to cisplatin by activating AMPK and suppressing the AKT signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hong-Bo Li ◽  
Jun-Kai Chen ◽  
Ze-Xin Su ◽  
Qing-Lin Jin ◽  
Li-Wen Deng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Mtor Signaling ◽  
Osteosarcoma Cell ◽  
Mtor Signaling Pathway ◽  
Osteosarcoma Cells ◽  
Related Proteins

Abstract Background Osteosarcoma is the most common primary bone tumor in children and adolescents. However, some patients with osteosarcoma develop resistance to chemotherapy, leading to a poor clinical prognosis. Hence, effective therapeutic agents that can improve the response to chemotherapy drugs to improve the prognosis of patients with osteosarcoma are urgently needed. Cordycepin has recently emerged as a promising antitumor drug candidate. This study aims to explore the effect of cordycepin in suppressing osteosarcoma in vivo and in vitro and the synergistic effect of cordycepin combined with cisplatin and to demonstrate the underlying molecular mechanism. Methods CCK-8 assay was performed to investigate the inhibition effect of cordycepin combined with cisplatin in osteosarcoma cell lines. The colony formation and invasion abilities were measured by colony formation assay and Transwell assay. Osteosarcoma cells apoptosis was detected by flow cytometry. Western blot analysis were used to detect the expression of cell apoptosis-related proteins and AMPK and AKT/mTOR signaling pathway-related proteins. Finally, we performed the in vivo animal model to further explore whether cordycepin and cisplatin exert synergistic antitumor effects. Results Notably, we found that treatment with cordycepin inhibited cell proliferation, invasion, and induced apoptosis in osteosarcoma cells in vitro and in vivo. Moreover, the combination of cordycepin and cisplatin led to marked inhibition of osteosarcoma cell proliferation and invasion and promoted osteosarcoma cell apoptosis in vitro and in vivo. Mechanistically, we demonstrated that cordycepin enhanced the sensitivity of osteosarcoma cells to cisplatin by activating AMPK and inhibiting the AKT/mTOR signaling pathway. Conclusions In brief, this study provides comprehensive evidence that cordycepin inhibits osteosarcoma cell growth and invasion and induces osteosarcoma cell apoptosis by activating AMPK and inhibiting the AKT/mTOR signaling pathway and enhances the sensitivity of osteosarcoma cells to cisplatin, suggesting that cordycepin is a promising treatment for osteosarcoma.

scholarly journals miR-193a-3p Mediates Placenta Accreta Spectrum Development by Targeting EFNB2 via Epithelial-Mesenchymal Transition Pathway Under Decidua Defect Conditions

2021 ◽  
Vol 7 ◽  
Author(s):  
Na Li ◽  
Rui Hou ◽  
Tian Yang ◽  
Caixia Liu ◽  
Jun Wei
Keyword(s):  
Conditioned Medium ◽  
Epithelial Mesenchymal Transition ◽  
Placenta Accreta ◽  
Migration And Invasion ◽  
Control Group ◽  
Mesenchymal Transition ◽  
Placenta Accreta Spectrum ◽  
Related Proteins ◽  
Cells Cultured

Objective: To clarify the role of microRNA-193a-3p (miR-193a-3p) in the pathogenesis of placenta accreta spectrum.Methods: The placental tissue expression levels of miR-193a-3p and Ephrin-B2 (EFNB2) were compared between a placenta accreta spectrum group and a control group. Transwell migration and invasion assays were used to verify the effect of miR-193a-3p and EFNB2 on HTR-8/SVneo cells cultured in human endometrial stromal cell (hESC)-conditioned medium. Epithelial-mesenchymal transition (EMT)-related proteins were examined by western blotting to establish whether the EMT pathway was altered in placenta accreta spectrum. To determine whether EFNB2 is a target gene of miR-193a-3p, luciferase activity assays were performed.Results: miR-193a-3p was upregulated but EFNB2 downregulated in the placenta accreta spectrum group and EFNB2 was a direct target of miR-193a-3p. Overexpression or inhibition of miR-193a-3p revealed that miR-193a-3p promoted the migration and invasion of HTR-8/SVneo cells cultured in hESC-conditioned medium. Furthermore, EMT was induced, as shown by increased N-cadherin, vimentin, MMP2, and MMP9 and decreased E-cadherin in the placenta accreta spectrum group and in HTR-8/SVneo cells transfected with miR-193a-3p mimics or si-EFNB2. The negative effect of miR-193a-3p inhibitor was reversed by co-transfection with si-EFNB2 in function studies and in analyses of EMT-related proteins in vitro.Conclusion: miR-193a-3p which upregulated in placenta accreta spectrum group increases HTR-8/SVneo cell migration and invasion by targeting EFNB2 via the EMT pathway under decidua defect conditions to lead to placenta accreta spectrum.

scholarly journals CHN1 promotes epithelial–mesenchymal transition via the Akt/GSK-3β/Snail pathway in cervical carcinoma

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Haoqi Zhao ◽  
Lan Wang ◽  
Shufang Wang ◽  
Xihua Chen ◽  
Min Liang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lymph Node ◽  
Signaling Pathway ◽  
Cervical Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Xenograft Tumor ◽  
Mesenchymal Transition ◽  
Gsk 3Β ◽  
Related Proteins

Abstract Background Metastasis and invasion are crucial in determining the mortality of cervical carcinoma (CC) patients. The epithelial–mesenchymal transition (EMT) is now a universal explanation for the mechanisms of tumor metastasis. Α-chimeric protein (α-chimaerin, CHN1) plays an important role in the regulation of signal transduction and development. However, the molecular regulatory relationships between CHN1 and CC progression in relation to EMT have not yet been identified. Methods The expression of CHN1 in CC tissues, adjacent tissues, and lymph node metastases from CC patients was detected by immunohistochemistry. Upregulation and knockdown of CHN1 were achieved by transfection of CC cells. The effect of CHN1 on cell proliferation was determined by CCK-8 and plate clone formation assays. Changes in migration and invasion capabilities were evaluated using scratch migration and transwell invasion assays. The effect of CHN1 overexpression and interference on xenograft tumor growth was determined by tumor weight and pathological analyses. The expression of EMT-related mRNAs was measured by qRT-PCR in transfected CC cells. EMT-related proteins and Akt/GSK-3β/Snail signaling pathway-related proteins were also evaluated by western blotting. Results CHN1 was overexpressed in CC tissues and was associated with lymph node metastasis and low survival in CC patients. Overexpression of CHN1 promoted cell proliferation, migration, and invasion in CC cells. In contrast, silencing of CHN1 inhibited these phenomena. Overexpression of CHN1 promoted tumor formation in an in vivo xenograft tumor mouse model, with increased tumor volumes and weights. In addition, CHN1 induced the expression of EMT-related transcription factors, accompanied by the decreased expression of epithelial markers and increased expression of mesenchymal markers. The Akt/GSK-3β/Snail signaling pathway was activated by overexpression of CHN1 in vitro, and activation of this pathway was inhibited by the signaling pathway inhibitor LY294002. Conclusion These results suggest that CHN1 promotes the development and progression of cervical carcinoma via the Akt/GSK-3β/Snail pathway by inducing EMT.

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