scholarly journals Ethanol extracted from radix of Actinidia chinensis inhibits human colon tumor through inhibiting Notch-signaling pathway

2020 ◽  
Author(s):  
Wanle Hu ◽  
Chenchen Wu ◽  
Chenchen Yuan ◽  
Minyuan Chen ◽  
Chun Jin ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Human Colon ◽  
Notch Signaling Pathway ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Actinidia Chinensis ◽  
Human Colon Cancer

Abstract Abstract: Background Colorectal cancer is one of the most common tumors, and its five-year survival is still very low despite of the advance of treatment strategies. The antitumor effect of ethanol extracted from radix of Actinidia chinensis (EERAC) were identified in human colon cancer cells, but the underlying mechanism remains unclear. Methods Cell proliferation, migration, and invasion were measured with CCK-8, wound healing, and transwell assays. Cell apoptosis and cycle were detected by flow cytometry. Western blotting and qRT-PCR were used to measure expression of target molecules. Xenograft tumor assay was applied to detect the influence of EERAC on tumor growth. Results In the present study, we found that EERAC inhibited the cell viability, migration, and invasion of SW480 cells in a concentration dependent manner, but promoted apoptosis and the cell percentage in S phase significantly. The suppression of notch-signaling pathway molecules (Notch1, Jagged1, and c-Myc) by EERAC was confirmed using western blotting and immunohistochemical staining. The significant inhibition of tumor growth by EERAC was also observed. Meanwhile, EERAC remarkably reversed the effects of MAML1 (activator of notch-signaling pathway) on cell survival of SW480. Conclusions Therefore, EERAC might be a promising chemotherapeutic agent for CRC treatment.

scholarly journals Ethanol Extracted from Radix of Actinidia Chinensis Inhibits Human Colon Tumor Through Inhibiting Notch-signaling Pathway

2021 ◽  
Vol 12 (3) ◽  
pp. 622-629
Author(s):  
Wanle Hu ◽  
Chenchen Wu ◽  
Chenchen Yuan ◽  
Minyuan Chen ◽  
Chun Jin ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Signaling Pathway ◽  
Human Colon ◽  
Notch Signaling Pathway ◽  
Colon Tumor ◽  
Actinidia Chinensis

scholarly journals SPON2 Is Upregulated through Notch Signaling Pathway and Promotes Tumor Progression in Gastric Cancer

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1439
Author(s):  
Hyeon-Gu Kang ◽  
Won-Jin Kim ◽  
Myung-Giun Noh ◽  
Kyung-Hee Chun ◽  
Seok-Jun Kim
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Notch Signaling Pathway ◽  
Migration And Invasion ◽  
Gene Assay ◽  
Gastric Cancer Progression

Spondin-2 (SPON2) is involved in cancer progression and metastasis of many tumors; however, its role and underlying mechanism in gastric cancer are still obscure. In this study, we investigated the role of SPON2 and related signaling pathway in gastric cancer progression and metastasis. SPON2 expression levels were found to be upregulated in gastric cancer cell lines and patient tissues compared to normal gastric epithelial cells and normal controls. Furthermore, SPON2 silencing was observed to decrease cell proliferation and motility and reduce tumor growth in xenograft mice. Conversely, SPON2 overexpression was found to increase cell proliferation and motility. Subsequently, we focused on regulatory mechanism of SPON2 in gastric cancer. cDNA microarray and in vitro study showed that Notch signaling is significantly correlated to SPON2 expression. Therefore, we confirmed how Notch signaling pathway regulate SPON2 expression using Notch signaling-related transcription factor interaction and reporter gene assay. Additionally, activation of Notch signaling was observed to increase cell proliferation, migration, and invasion through SPON2 expression. Our study demonstrated that Notch signaling-mediated SPON2 upregulation is associated with aggressive progression of gastric cancer. In conclusion, we suggest upregulated SPON2 via Notch signaling as a potential target gene to inhibit gastric cancer progression.

HOXA3 promotes tumor growth of human colon cancer through activating EGFR/Ras/Raf/MEK/ERK signaling pathway

2017 ◽  
Vol 119 (3) ◽  
pp. 2864-2874 ◽  
Author(s):  
Xianxiang Zhang ◽  
Guangwei Liu ◽  
Lei Ding ◽  
Tao Jiang ◽  
Shihong Shao ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Human Colon ◽  
Erk Signaling ◽  
Human Colon Cancer

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 MicroRNA-140-5p inhibits cell proliferation, migration and promotes cell apoptosis in gastric cancer through the negative regulation of THY1-mediated Notch signaling

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Kun Wu ◽  
Jun Zou ◽  
Chao Lin ◽  
Zhi-Gang Jie
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Expression Profiles ◽  
Differentially Expressed Gene ◽  
Notch Signaling Pathway ◽  
Differentially Expressed ◽  
Migration And Invasion ◽  
Enhanced Expression

Abstract Studies have highlighted the importance of microRNAs (miRs) in the development of various cancers, including gastric cancer (GC), a commonly occurring malignancy, accompanied by high recurrence and metastasis rate. The aim of the current study was to investigate the role of miR-140-5p in GC. Microarray expression profiles were initially employed to screen the differentially expressed gene related to GC, and the miR regulating the gene was predicted accordingly. The data obtained indicated that thymus cell antigen 1 (THY1) was differentially expressed in GC and confirmed to be a target gene of miR-140-5p. Poorly expressed miR-140-5p and highly expressed THY1 were observed in the GC tissues. SGC-7901 cells were treated with miR-140-5p mimic/inhibitor, siRNA against THY1 and siRNA against Notch1 in order to determine their regulatory roles in GC cell activities. The relationship of miR-140-5p, THY1 and the Notch signaling pathway was subsequently identified. Moreover, cell proliferation, migration, invasion and apoptosis were determined using 3-(4,5-dimethylthiazol-2-yl)-5(3-carboxymethonyphenol)-2-(4-sulfophenyl)-2H-tetrazolium (MTS), wound-healing, transwell assay and flow cytometry, respectively. The overexpression of miR-140-5p and silencing of THY1 resulted in a diminished expression of the Notch signaling pathway-related proteins, as well as inhibited proliferation, migration and invasion of GC cells, enhanced expression of pro-apoptotic proteins in addition to elevated apoptosis rate. Taken together, the present study suggests that miR-140-5p directly targets and negatively regulates THY1 expression and inhibits activation of the Notch signaling pathway, whereby the up-regulation of miR-140-5p inhibits development of GC, highlighting the promise of miR-140-5p as a potential target for GC treatment.

scholarly journals Astragalus Polysaccharide RAP Induces Macrophage Phenotype Polarization to M1 via the Notch Signaling Pathway

Molecules ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 2016 ◽  
Author(s):  
Wei Wei ◽  
Zhi-Peng Li ◽  
Zhao-Xiang Bian ◽  
Quan-Bin Han
Keyword(s):  
Tumor Growth ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Macrophage Polarization ◽  
Notch Signaling Pathway ◽  
Raw264.7 Cells ◽  
Control Group ◽  
Macrophage Phenotype ◽  
Astragalus Polysaccharide ◽  
M1 Phenotype

Macrophages occur in polarized phenotypes, whose characteristics determine the role they play in tumor growth. The M1 phenotype macrophages promote tumoricidal responses and suppress tumor growth. Our previous study showed that a polysaccharide isolated from Radix Astragali, named RAP, was itself non-cytotoxic but induced RAW264.7 cells’ cytotoxicity against cancer cells. The current study was undertaken to determine its mechanism. Series studies was conducted to show that RAP is able to induce much higher gene expression of M1 markers, including iNOS, IL-6, TNF-a, and CXCL10, compared with the control group. When RAP-induced BMDMs were transplanted together with 4T1 tumor cells in BALB/c mice, both tumor volume and tumor weight decreased. Further studies indicated that RAP induces the Notch signaling pathway in RAW264.7 cells. The function of Notch signaling in macrophage polarization was confirmed by using γ-secretase inhibitor. These results suggested that Astragalus polysaccharide RAP induces macrophage’s polarization to M1 phenotype via the Notch signaling pathway.

scholarly journals microRNA-1271-5p/TIAM1 suppresses the progression of ovarian cancer through inactivating Notch signaling pathway

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Feng-Juan Han ◽  
Jia Li ◽  
Ying Shen ◽  
Ying Guo ◽  
Yi-Chao Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Target Gene ◽  
Notch Signaling Pathway ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Western Blot Assay

Abstract Objective Ovarian cancer (OC) has been regarded as the most malignant gynecological neoplasm and often confers grave outcomes owing to the frequent metastasis and high recurrence. A previous study has demonstrated that miR-1271-5p is implicated in OC progression, however, the possible mechanism of it remains unknown. The purpose of this investigation was to explore how miR-1271-5p regulates the progression of OC. Methods Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were employed to analyze the differentially expressed miRNAs or genes as well as their corresponding prognostic values. miR-1271-5p expression in OC cells was examined by qRT-PCR. Cell counting kit 8 (CCK-8), colony formation, and transwell tests were conducted to evaluate the proliferation, migration and invasion potentials. Bioinformatics prediction and luciferase activity analysis were utilized to predict and verify the target gene of miR-1271-5p. Western blot assay was carried out to measure protein expression. Results miR-1271-5p was significantly decreased in OC and its down-regulation was associated with the grave outcome of OC patients. Upregulation of miR-1271-5p inhibited cell viability, but miR-1271-5p knockdown promoted the proliferation of OC cells. TIAM1 was a direct target gene of miR-1271-5p and expressed in OC tissues at higher level. High expression of TIAM1 induced the poorer prognosis of patients with OC. Further functional analyses showed that the suppressive role of miR-1271-5p on OC cell malignant behaviors was overturned by the upregulation of TIAM1. The protein levels of Cyclin D1, HES1, NOTCH and NUMB were remarkably changed due to the abnormal expression of miR-1271-5p and TIAM1. Conclusion To sum up, miR-1271-5p inhibits proliferation, invasion and migration of OC cells by directly repressing TIAM1 to inactivate the Notch signaling pathway, which provides an alternative therapeutic candidate for the advancement of OC treatment.

Sign in / Sign up

Export Citation Format

Share Document