scholarly journals Antitumor Effect of Saikosaponin A on Human Neuroblastoma Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Tan Cheng ◽  
Muying Ying
Keyword(s):  
Protein Expression ◽  
Epithelial Mesenchymal Transition ◽  
Neuroblastoma Cells ◽  
Metastatic Tumor ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Related Protein ◽  
Human Neuroblastoma ◽  
Mesenchymal Transition ◽  
Saikosaponin A

Objective. Neuroblastoma (NB) is a highly metastatic tumor in children that develops in the sympathetic nervous system and has a low curative rate. Saikosaponin A (SSA), an active ingredient isolated from the root of Radix Bupleuri, is a natural compound with various pharmacological activities and shows good application prospects in antitumors. This study investigated the antihuman NB activity of SSA and underlying mechanisms associated with its actions. Materials and Methods. The MTT method was used to detect the activity of SSA in inhibiting human NB cell SK-N-AS proliferation. Cell morphology was observed. The flow cytometry technology was used in analyzing the cell apoptosis rate. The Transwell assay evaluated cell migration and invasion following SSA treatment, apoptosis-related protein expression, and angiogenesis-related protein expression, and EMT-related proteins were detected by western blot analysis. Results. SSA showed an inhibitory effect on SK-N-AS cells with the IC50 values of 14.14 μM at 24 h and 12.41 μM at 48 h. Results indicated that SSA has proapoptotic activity, and its proapoptotic activity is positively correlated with the Bax/Bcl-2/caspase-9/caspase-7/PARP pathway. Furthermore, SSA inhibited the invasion and migration of SK-N-AS cells via regulating the angiogenesis-related VEGFR2/Src/Akt pathway and the epithelial-mesenchymal transition- (EMT-) related protein expression. Conclusion. SSA exerts an antihuman NB effect and thus provides foundations for NB treatment.

scholarly journals Silencing of the TROP2 gene suppresses proliferation and invasion of hepatocellular carcinoma HepG2 cells

2019 ◽  
Vol 47 (3) ◽  
pp. 1319-1329 ◽  
Author(s):  
Jian Zhang ◽  
Hai Ma ◽  
Liu Yang ◽  
Hongchun Yang ◽  
Zhenxing He
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Human Trophoblast ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Proliferation And Invasion

Objectives Overexpression of human trophoblast cell surface antigen 2 (Trop2) has been observed in many cancers; however, its roles in proliferation, apoptosis, migration, and invasion of hepatocellular carcinoma (HCC) remain unclear. Thus, this study aimed to characterize the function of Trop2 in HCC. Methods Trop2 protein expression was detected by immunohistochemistry in HCC tissues. Cell proliferation, apoptosis, and invasion were respectively measured by CCK-8, flow cytometry, Transwell, and wound healing assays. Expression levels of epithelial–mesenchymal transition-related proteins and Trop2 protein in HCC cell lines were detected by western blotting after silencing of the TROP2 gene. Results Trop2 protein was highly expressed in HCC tissues and HCC cell lines. Trop2 mRNA and protein expression levels decreased in HepG2 and HCCLM3 cells after transfection with Trop2 siRNA. Silencing of the TROP2 gene in HepG2 and HCCLM3 cells strongly inhibited cell proliferation and migration, while enhancing cell apoptosis. Investigation of the molecular mechanism revealed that silencing of the TROP2 gene suppressed epithelial–mesenchymal transition of HepG2 and HCCLM3 cells. Conclusions The results of the present study may improve understanding of the role of Trop2 in regulation of cell proliferation and invasion, and may aid in development of novel therapy for HCC.

Prognostic importance of epithelial-mesenchymal transition-related protein expression in gastric carcinoma

2009 ◽  
Vol 54 (4) ◽  
pp. 442-451 ◽  
Author(s):  
Min A Kim ◽  
Hye Seung Lee ◽  
Hee Eun Lee ◽  
Ji Hun Kim ◽  
Han-Kwang Yang ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Protein Expression ◽  
Epithelial Mesenchymal Transition ◽  
Related Protein ◽  
Mesenchymal Transition ◽  
Prognostic Importance

scholarly journals Prognostic impact of EMT (epithelial-mesenchymal-transition)-related protein expression in endometrial cancer

2013 ◽  
Vol 14 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Yoshimichi Tanaka ◽  
Yoshito Terai ◽  
Hiroshi Kawaguchi ◽  
Satoe Fujiwara ◽  
Saha Yoo ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Protein Expression ◽  
Epithelial Mesenchymal Transition ◽  
Prognostic Impact ◽  
Related Protein ◽  
Mesenchymal Transition

scholarly journals Triptolide suppresses the growth and metastasis of non-small cell lung cancer by inhibiting β-catenin-mediated epithelial–mesenchymal transition

2021 ◽  
Author(s):  
Qiu-di Deng ◽  
Xue-ping Lei ◽  
Yi-hang Zhong ◽  
Min-shan Chen ◽  
Yuan-yu Ke ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Small Cell ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Small Cell Lung ◽  
Mesenchymal Transition

AbstractNon-small cell lung cancer (NSCLC) is characterized by a high incidence of metastasis and poor survival. As epithelial–mesenchymal transition (EMT) is well recognized as a major factor initiating tumor metastasis, developing EMT inhibitor could be a feasible treatment for metastatic NSCLC. Recent studies show that triptolide isolated from Tripterygium wilfordii Hook F attenuated the migration and invasion of breast cancer, colon carcinoma, and ovarian cancer cells, and EMT played important roles in this process. In the present study we investigated the effect of triptolide on the migration and invasion of NSCLC cell lines. We showed that triptolide (0.5, 1.0, 2.0 nM) concentration-dependently inhibited the migration and invasion of NCI-H1299 cells. Triptolide treatment concentration-dependently suppressed EMT in NCI-H1299 cells, evidenced by significantly elevated E-cadherin expression and reduced expression of ZEB1, vimentin, and slug. Furthermore, triptolide treatment suppressed β-catenin expression in NCI-H1299 and NCI-H460 cells, overexpression of β-catenin antagonized triptolide-caused inhibition on EMT, whereas knockout of β-catenin enhanced the inhibitory effect of triptolide on EMT. Administration of triptolide (0.75, 1.5 mg/kg per day, ip, every 2 days) for 18 days in NCI-H1299 xenograft mice dose-dependently suppressed the tumor growth, restrained EMT, and decreased lung metastasis, as evidence by significantly decreased expression of mesenchymal markers, increased expression of epithelial markers as well as reduced number of pulmonary lung metastatic foci. These results demonstrate that triptolide suppresses NSCLC metastasis by targeting EMT via reducing β-catenin expression. Our study implies that triptolide may be developed as a potential agent for the therapy of NSCLC metastasis.

scholarly journals MiR-200b Suppresses Gastric Cancer Cell Migration and Invasion by Inhibiting NRG1 through ERBB2/ERBB3 Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Tonglei Xu ◽  
Fangliang Xie ◽  
Dazhou Xu ◽  
Weidong Xu ◽  
Xuming Ge ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Neuregulin 1 ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Erbb3 Signaling

Purpose. Accumulating evidence indicates that miRNAs (miRs) play crucial roles in the modulation of tumors development. However, the accurately mechanisms have not been entirely clarified. In this study, we aimed to explore the role of miR-200b in the development of gastric cancer (GC). Methods. Western blot and RT-PCR were applied to detect epithelial-mesenchymal transition (EMT) marker expression and mRNA expression. Transwell assay was used for measuring the metastasis and invasiveness of GC cells. TargetScan system, luciferase reporter assay, and rescue experiments were applied for validating the direct target of miR-200b. Results. MiR-200b was prominently decreased in GC tissues and cells, and its downregulation was an indicator of poor prognosis of GC patients. Reexpression of miR-200b suppressed EMT along with GC cell migration and invasion. Neuregulin 1 (NRG1) was validated as the target of miR-200b, and it rescued miR-200b inhibitory effect on GC progression. In GC tissues, the correlation of miR-200b with NRG1 was inverse. Conclusion. MiR-200b suppressed EMT-related migration and invasion of GC through the ERBB2/ERBB3 signaling pathway via targeting NRG1.

scholarly journals Polygonum Barbatum Extract Reduces Colorectal Cancer Cell Proliferation, Migration, Invasion, and Epithelial-mesenchymal Transition via Regulation of the YAP and β-catenin Pathways

2021 ◽  
Author(s):  
Pi-Kai Chang ◽  
I-Chuan Yen ◽  
Wei-Cheng Tsai ◽  
Shih-Yu Lee
Keyword(s):  
Extracellular Matrix ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colony Formation ◽  
Epithelial Mesenchymal Transition ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Pathway Enrichment Analysis ◽  
Human Colon Cancer ◽  
Mesenchymal Transition

Abstract BackgroundColorectal cancer (CRC) is the third most common cancer worldwide, but the development of novel therapeutics for CRC remains a challenge. Polygonum barbatum has anticancer potential, but its mechanism of action requires further investigation. This study was designed to investigate the inhibitory effect of Polygonum barbatum on human CRC cells. The HPLC fingerprints of the Polygonum barbatum extract (PBE) and quercetin standard were determined using analytical RP-HPLC and evaluations were completed using the human colon cancer cell line HCT-116 (KRASG13D mutation) and HT-29 cells. After treatment with PBE, cell viability, colony formation, migration, invasion, and apoptosis were analyzed using CCK-8, colony formation, wound healing, Transwell invasion, and flow cytometry assays, respectively. RNA-sequencing, western blotting, and co-immunoprecipitation were also used to analyze changes in the whole-transcriptome of these cells and identify possible mechanisms of action for PBE in CRC cells. ResultsPBE significantly reduced CRC cell growth, migration, and invasion, and Gene Ontology analysis showed that the genes responsible for extracellular matrix organization, cell motility, and cell growth were suppressed by PBE. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of the differentially expressed genes revealed that PBE treatment exerted a significant effect on the extracellular matrix interaction and focal adhesion pathways. Consistently, epithelial-to-mesenchymal transition markers, including N-cadherin, vimentin, SLUG, and SNAIL, were also all shown to be regulated by PBE. These effects were associated with blockade of the Yes-associated protein and the GSK3β/β-catenin axis.ConclusionPolygonum barbatum extract exerts a significant inhibitory effect on CRC cells and may be potentially applicable in clinical trials.

Epithelial-mesenchymal transition-related protein expression in biliary epithelial cells associated with hepatolithiasis

2014 ◽  
Vol 29 (2) ◽  
pp. 395-402 ◽  
Author(s):  
Rohyun Sung ◽  
Sang Hwa Lee ◽  
Meiying Ji ◽  
Joung-Ho Han ◽  
Min Ho Kang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Epithelial Mesenchymal Transition ◽  
Related Protein ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

scholarly journals Gemifloxacin, a Fluoroquinolone Antimicrobial Drug, Inhibits Migration and Invasion of Human Colon Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Jung-Yu Kan ◽  
Ya-Ling Hsu ◽  
Yen-Hsu Chen ◽  
Tun-Chieh Chen ◽  
Jaw-Yuan Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Migration ◽  
Nuclear Translocation ◽  
Epithelial Mesenchymal Transition ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Human Colon Cancer ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion

Gemifloxacin (GMF) is an orally administered broad-spectrum fluoroquinolone antimicrobial agent used to treat acute bacterial exacerbation of pneumonia and bronchitis. Although fluoroquinolone antibiotics have also been found to have anti-inflammatory and anticancer effects, studies on the effect of GMF on treating colon cancer have been relatively rare. To the best of our knowledge, this is the first report to describe the antimetastasis activities of GMF in colon cancer and the possible mechanisms involved. Results have shown that GMF inhibits the migration and invasion of colon cancer SW620 and LoVo cells and causes epithelial mesenchymal transition (EMT). In addition, GMF suppresses the activation of NF-κB and cell migration and invasion induced by TNF-αand inhibits the TAK1/TAB2 interaction, resulting in decreased IκB phosphorylation and NF-κB nuclear translocation in SW620 cells. Furthermore, Snail, a critical transcriptional factor of EMT, was downregulated after GMF treatment. Overexpression of Snail by cDNA transfection significantly decreases the inhibitory effect of GMF on EMT and cell migration and invasion. In conclusion, GMF may be a novel anticancer agent for the treatment of metastasis in colon cancer.

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