scholarly journals Cucurbitacin E inhibits osteosarcoma cells proliferation and invasion through attenuation of PI3K/AKT/mTOR signalling pathway

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Ying Wang ◽  
Shumei Xu ◽  
Yaochi Wu ◽  
Junfeng Zhang
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Signalling Pathway ◽  
Cell Counting ◽  
Cell Cycle Distribution ◽  
Mesenchymal Transition ◽  
Cucurbitacin E ◽  
Mtor Signalling ◽  
Mtor Signalling Pathway

Cucurbitacin E (CuE), a potent member of triterpenoid family isolated from plants, has been confirmed as an antitumour agent by inhibiting proliferation, migration and metastasis in diverse cancer. However, the effects and mechanisms of CuE on osteosarcoma (OS) have not been well understood. The present study aimed to test whether CuE could inhibit growth and invasion of OS cells and reveal its underlying molecular mechanism. After various concentrations of CuE treatment, the anti-proliferative effect of CuE was assessed using the cell counting Kit-8 assay. Flow cytometry analysis was employed to measure apoptosis of OS cells. Cell cycle distribution was analysed by propidium iodide staining. Transwell assay was performed to evaluate the effect of CuE on invasion potential of OS cells. The protein levels were measured by western blot. In addition, the potency of CuE on OS cells growth inhibition was assessed in vivo. Our results showed that CuE inhibited cell growth and invasion, induced a cell cycle arrest and triggered apoptosis and modulated the expression of cell growth, cell cycle and cell apoptosis regulators. Moreover, CuE inhibited the PI3K/Akt/mTOR pathway and epithelial–mesenchymal transition (EMT), which suppressed the invasion and metastasis of OS. In addition, we also found that CuE inhibited OS cell growth in vivo. Taken together, our study demonstrated that CuE could inhibit OS tumour growth and invasion through inhibiting the PI3K/Akt/mTOR signalling pathway. Our findings suggest that CuE can be considered to be a promising anti-cancer agent for OS.

Effects of L.   paracasei subp. paracasei X12 on cell cycle of colon cancer HT-29 cells and regulation of mTOR signalling pathway

2016 ◽  
Vol 21 ◽  
pp. 431-439 ◽  
Author(s):  
Lei Huang ◽  
Yu-Juan Shan ◽  
Can-Xia He ◽  
Ming-Hua Ren ◽  
Pei-Jun Tian ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Signalling Pathway ◽  
Ht 29 ◽  
Mtor Signalling ◽  
Mtor Signalling Pathway

scholarly journals MicroRNA‑138 modulates glioma cell growth, apoptosis and invasion through the suppression of the AKT/mTOR signalling pathway by targeting CREB1

2020 ◽  
Vol 44 (6) ◽  
pp. 2559-2568
Author(s):  
Chi Zhang ◽  
Qi Wang ◽  
Xiaowen Zhou ◽  
Lei Zhang ◽  
Ying Yao ◽  
...  
Keyword(s):  
Cell Growth ◽  
Glioma Cell ◽  
Signalling Pathway ◽  
Mtor Signalling ◽  
Mtor Signalling Pathway

scholarly journals FZD2 Promotes TGF-β-Induced Epithelial-to-Mesenchymal Transition in Breast Cancer via Activating Notch Signaling Pathway

2020 ◽  
Author(s):  
Dilihumaer Tuluhong ◽  
Tao Chen ◽  
Jingjie Wang ◽  
Huijuan Zeng ◽  
Hanjun Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Tgf Β1

Abstract Background Breast cancer (BC) is one of the commonest female cancers, which is characterized with high incidence. Although treatments have been improved, the prognosis of BC patients in advanced stages remains unsatisfactory. Thus, exploration of the molecular mechanisms underneath BC progression is necessary to find novel therapeutic methods. Frizzled class receptor (FZD2) belongs to Frizzled family, which has been proven to promote cell growth and invasion in various human cancers. The purpose of our study was to detect the functions of FZD2 and explore its mechanism in BC. Methods The level of FZD2 was measured in BC tissues by quantitative realtime polymerase chain reaction (qRT-PCR), western blot, immunohistochemistry (IHC) respectively. Cell Counting Kit-8 (CCK-8), standard colony formation, transwell aasays, wound healing and flow cytometry experiments were adopted separately to test cell viability, invasion, migration, apoptosis and cell cycle distribution. Epithelial-mesenchymal transition (EMT) biomarker were determined by using Immunofluorescence assay. Xenograft tumorigenicity assay was performed to assess the effect of FZD2 on tumor growth in vivo. Results We determined that FZD2 mRNA and protein expression was abundant in BC tissues. Moreover, high level of FZD2 had significant correlation with poor prognosis. In vitro functional assays revealed that silencing of FZD2 had suppressive effects on BC cell growth, migration and invasion. Animal study further demonstrated that FZD2 silencing inhibited BC cell growth in vivo. In addition, FZD2 induced EMT in BC cells in a transforming growth factor (TGF)-β1-dependent manner. Mechanistically, knockdown of FZD2 led to the inactivation of Notch signaling pathway. Conclusion Based on all these data, we concluded that FZD2 facilitates BC progression and promotes TGF-β1-inudced EMT process through activating Notch signaling pathway.

scholarly journals FZD2 promotes TGF-β-induced epithelial-to-mesenchymal transition in breast cancer via activating notch signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dilihumaer Tuluhong ◽  
Tao Chen ◽  
Jingjie Wang ◽  
Huijuan Zeng ◽  
Hanjun Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Notch Signaling Pathway ◽  
Cell Counting ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Tgf Β1

Abstract Background Breast cancer (BC) is one of the commonest female cancers, which is characterized with high incidence. Although treatments have been improved, the prognosis of BC patients in advanced stages remains unsatisfactory. Thus, exploration of the molecular mechanisms underneath BC progression is necessary to find novel therapeutic methods. Frizzled class receptor 2 (FZD2) belongs to Frizzled family, which has been proven to promote cell growth and invasion in various human cancers. The purpose of our current study was to detect the functions of FZD2 in BC and explore its underlying molecular mechanism. Methods The level of FZD2 was measured in BC tissues by quantitative real-time polymerase chain reaction (qRT-PCR), western blot, immunohistochemistry (IHC), respectively. Cell Counting Kit-8 (CCK-8), colony formation assay, transwell assays, wound healing assay and flow cytometry analyses were separately conducted to detect cell viability, invasion, migration, apoptosis and cell cycle distribution. The levels of Epithelial-mesenchymal transition (EMT) biomarkers were examined by using Immunofluorescence assay. Xenograft tumorigenicity assay was performed to assess the effect of FZD2 on tumor growth in vivo. Results FZD2 mRNA and protein expression was abundant in BC tissues. Moreover, high level of FZD2 had significant correlation with poor prognosis in BC patients. In vitro functional assays revealed that silencing of FZD2 had suppressive effects on BC cell growth, migration and invasion. Animal study further demonstrated that FZD2 silencing inhibited BC cell growth in vivo. In addition, FZD2 induced EMT process in BC cells in a transforming growth factor (TGF)-β1-dependent manner. Mechanistically, knockdown of FZD2 led to the inactivation of Notch signaling pathway. Conclusion FZD2 facilitates BC progression and promotes TGF-β1-inudced EMT process through activating Notch signaling pathway.

scholarly journals Inhibitory role of circRNA_100395 in the proliferation and metastasis of prostate cancer cells

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052199221
Author(s):  
Haitian He ◽  
Jianhua Li ◽  
Mayao Luo ◽  
Qiang Wei
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Counting ◽  
Cell Cycle Distribution ◽  
Prostate Cancer Cells ◽  
Mesenchymal Transition ◽  
Endogenous Expression ◽  
Proliferation And Metastasis

Objective Circular RNAs (circRNAs) are non-coding RNAs with high cancer-specific expression and the potential for regulating tumorigenesis. CircRNA_100395 is expressed at low levels in many cancers and is involved in the regulation of tumor cell proliferation and metastasis. However, its expression and function in prostate cancer remain unclear. Methods Endogenous expression levels of circRNA_100395 and microRNA-1228 (miR-1228) in prostate cancer tissue samples and cell lines were detected by quantitative reverse transcription-polymerase chain reaction. Cell proliferation, invasion, and migration, cell cycle distribution, and epithelial–mesenchymal transition (EMT) were analyzed in circRNA_100395-overexpressing prostate cancer cells by Cell Counting Kit-8, flow cytometry, Transwell assay, and western blotting, respectively. Results CircRNA_100395 expression was downregulated in cancerous prostate tissues relative to adjacent normal tissues. CircRNA_100395 expression was negatively correlated with tumor size, Gleason score, tumor stage, and lymph node metastasis. Moreover, circRNA_100395 overexpression inhibited cell proliferation, altered cell cycle distribution, reduced cell migration and invasion abilities, and suppressed EMT in prostate cancer cells. Moreover, miR-1228 was a direct downstream target of circRNA_100395, and the anti-tumor ability of circRNA_100395 was significantly reversed by miR-1228. Conclusion This study identified circRNA_100395 as an anti-tumor circRNA and a potential therapeutic target for prostate cancer.

scholarly journals Circ_0082182 promotes oncogenesis and metastasis of colorectal cancer in vitro and in vivo by sponging miR-411 and miR-1205 to activate the Wnt/β-catenin pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Ruijie Liu ◽  
Ping Deng ◽  
Yonglian Zhang ◽  
Yonglan Wang ◽  
Cuiping Peng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Mesenchymal Transition

Abstract Background Circular RNAs (circRNAs) are a class of endogenous single-strand RNA transcripts with crucial regulation in human cancers. The objective of this study is to investigate the role of circ_0082182 in CRC and its specific functional mechanism. Methods The quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure the levels of circ_0082182, microRNA-411 (miR-411) and microRNA-1205 (miR-1205). Cell proliferation was detected by Cell counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was used for determining cell cycle and cell apoptosis. Cell apoptosis was also assessed by caspase3 and caspase9 activities. Cell migration and invasion were examined using scratch assay and transwell assay. The interaction between circ_0082182 and miRNA was validated by the dual-luciferase reporter and biotinylated RNA pull-down assays. Wnt/β-catenin pathway and epithelial-mesenchymal transition (EMT)-associated proteins were quantified by Western blot. Xenograft model was established for the research of circ_0082182 in vivo. Results Circ_0082182 was upregulated in CRC and could predict the poor prognosis of CRC patients. Functionally, circ_0082182 promoted CRC cell proliferation, cell cycle progression, and metastasis while inhibited apoptosis. Subsequently, circ_0082182 was shown to act as the sponges of miR-411 and miR-1205. MiR-411 and miR-1205 were identified as tumor inhibitors in CRC. Furthermore, circ_0082182 promoted the CRC progression via sponging miR-411 and miR-1205. Moreover, circ_0082182 facilitated the Wnt/β-catenin pathway and EMT process by targeting miR-411 and miR-1205. In vivo, circ_0082182 accelerated the CRC tumorigenesis and EMT process by activating the Wnt/β-catenin pathway by downregulating the expression of miR-411 or miR-1205. Conclusion This study showed that circ_0082182 functioned as an oncogene in the developing process of CRC by sponging miR-411 or miR-1205 to activate the Wnt/β-catenin pathway. Circ_0082182 might be a molecular target in the diagnosis and treatment of CRC.

scholarly journals circHUWE1 Exerts an Oncogenic Role in Inducing DDP-Resistant NSCLC Progression Depending on the Regulation of miR-34a-5p/TNFAIP8

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Xueliang Yang ◽  
Quan Sun ◽  
Yongming Song ◽  
Wenli Li
Keyword(s):  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Cell Cycle Distribution ◽  
Necrosis Factor Alpha ◽  
Induced Apoptosis

Background. Circular RNAs (circRNAs) are reported as competing endogenous RNAs (ceRNAs) and play key roles in non-small-cell lung cancer (NSCLC) progression. Thus, this study was aimed at clarifying underlying molecular mechanisms of circHUWE1 in NSCLC. Methods. The quantitative real-time polymerase chain reaction (RT-qPCR) and western blot analyses were used for examining circHUWE1, microRNA-34a-5p (miR-34a-5p), and tumor necrosis factor alpha-induced protein 8 (TNFAIP8). IC50 of cisplatin (DDP) in A549/DDP and H1299/DDP cells and cell viability were analyzed by the Cell Counting Kit 8 (CCK-8) assay. Colony forming assay was performed to assess colony forming ability. Cell apoptosis and cell cycle distribution were determined by flow cytometry. Migrated and invaded cell numbers were examined by transwell assay. The association among circHUWE1, miR-34a-5p, and TNFAIP8 was analyzed by dual-luciferase reporter and RNA immunoprecipitation assays. A xenograft experiment was applied to clarify the functional role of circHUWE1 in vivo. Results. circHUWE1 was upregulated in NSCLC tissues and cells, especially in DDP-resistant groups. circHUWE1 downregulation inhibited DDP resistance, proliferation, migration, and invasion while it induced apoptosis and cell cycle arrest of DDP-resistant NSCLC cells, which was overturned by silencing of miR-34a-5p. TNFAIP8 was a functional gene of miR-34a-5p, and the suppressive effects of miR-34a-5p overexpression on DDP-resistant NSCLC progression were dependent on the suppression of TNFAIP8. circHUWE1 inhibition also delayed tumor growth of DDP-resistant NSCLC cells. Conclusion. circHUWE1 functioned as a promoter in DDP-resistant NSCLC by interaction with miR-34a-5p-TNFAIP8 networks, providing novel insight into DDP-resistant NSCLC diagnosis and treatment.

scholarly journals Fenofibrate Exerts Antitumor Effects in Colon Cancer via Regulation of DNMT1 and CDKN2A

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Rui Kong ◽  
Nan Wang ◽  
Wei Han ◽  
Wen Bao ◽  
Jie Lu
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Epigenetic Therapy ◽  
Cell Cycle Distribution ◽  
Peroxisome Proliferator ◽  
Antitumor Effects ◽  
Mesenchymal Transition

Peroxisome proliferator-activated receptor alpha (PPARA) is the molecular target of fibrates commonly used to treat dyslipidemia and diabetes. Recently, the potential role of PPARA in other pathological conditions, such as cancers, has been recognized. Here, using bioinformatics analysis, we found that PPARA was expressed at relatively low levels in pancancers, and Kaplan-Meier analyses revealed that high PPARA protein expression was correlated with better survival of patients with colon cancer. In vitro experiments showed that fenofibrate regulated cell cycle distribution, promoted apoptosis, and suppressed cell proliferation and epithelial mesenchymal transition by activating PPARA. PPARA activation inhibited DNMT1 activity and abolished methylation-mediated CDKN2A repression. Downregulation of cyclin-CDK complexes led to the restoration of CDKN2A, which caused cell cycle arrest in the G1 phase via regulation of the CDKN2A/RB/E2F pathway. Finally, we demonstrated that fenofibrate administration inhibited tumor growth and DNMT1 activity in vivo. The PPARA agonist, fenofibrate, might serve as an applicable agent for epigenetic therapy of colon cancer patients.

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