scholarly journals Analysis of Molecular Mechanism of YiqiChutan Formula Regulating DLL4-Notch Signaling to Inhibit Angiogenesis in Lung Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jiayin Li ◽  
Rui Han ◽  
Jing Li ◽  
Linzhu Zhai ◽  
Xinying Xie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Notch Signaling ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Human Lung ◽  
Carcinoma Cell ◽  
Treated Group ◽  
Control Group ◽  
Notch 1 ◽  
Transplanted Tumor

In order to explore the specific mechanism of YiqiChutan formula (YQCTF) in inhibiting the angiogenesis of lung cancer and its relationship with delta-like ligand 4- (DLL4-) Notch signaling, 30 healthy BALB/c-nu/nu rats were selected and divided into three groups: A549 group (implanted with lung adenocarcinoma cell line A549), NCI-H460 group (implanted with human lung large-cell carcinoma cell line NCI-H460), and NCI-H446 group (implanted with human lung small cell carcinoma cell line NCI-H446) for constructing lung cancer transplanted tumor models. After modeling, the group treated with normal saline was taken as control group, 200 mg/kg of YQCTF was adopted for intervention, and the tumor volume and growth inhibition rate were compared with the vascular targeted inhibitor Sorafenib. HE staining, CD31 fluorescent antibody staining, and microelectron microscopy were adopted to observe the neovascular endothelial cells of the transplanted tumor. The expression of VEGF, HIF-1α, DLL4, and Notch-1 in the transplanted tumors in each group was detected by Western blot and RT-PCR at the protein level or mRNA level. Compared with the control group, the YQCTF-treated group had obvious inhibitory effect on lung cancer transplanted tumor and lung cancer angiogenesis. In the YQCTF-treated group, the density of angiogenesis decreased significantly and the vascular lumen structure also decreased, and the expression levels of VEGF, HIF-1α, DLL4, and Notch-1 in the YQCTF-treated group were all lower than those in the control group. YQCTF could inhibit the growth of lung cancer transplanted tumor through antiangiogenesis, and it could also reduce the amount of angiogenesis in lung cancer transplanted tumor. In addition, the generation of lumen structure was also hindered, which was realized through the VEGF signaling pathway and DLL4-Notch signaling pathway.

scholarly journals Cytotoxic and Apoptotic Effects of Ferulic Acid on Renal Carcinoma Cell Line (ACHN)

2020 ◽  
Vol 15 (4) ◽  
Author(s):  
Mahshid Naseri Karimvand ◽  
Hadi Kalantar ◽  
Mohammad Javad Khodayar
Keyword(s):  
Gene Expression ◽  
Ferulic Acid ◽  
Cancer Cells ◽  
Cell Line ◽  
Mtt Assay ◽  
Renal Carcinoma ◽  
Carcinoma Cell ◽  
Treated Group ◽  
Control Group ◽  
Renal Carcinoma Cell Line

Background: Polyphenolic compounds have anti-proliferative effects and can trigger apoptosis in cancer cells. Ferulic acid is excessively found in various herbal products and fruits. Ferulic acid plays a role in the treatment of neurodegenerative diseases, cancer, diabetes, cardiovascular disease, inflammation, and bacterial and viral infections. Objectives: The purpose of this study was to evaluate the anticancer effect of ferulic acid on renal carcinoma cells (ACHN). Methods: To assess the anti-proliferative effect of ferulic acid, the renal carcinoma cell line (ACHN) was treated with different ferulic acid concentrations (10, 20, 40, 80, and 160 μM) for 24, 48, and 72 hours. Cell viability was measured using the MTT assay. The apoptosis of cancer cells was evaluated by flow cytometry and real-time PCR. Results: The IC50 of ferulic acid against ACHN cells was determined to be 30 μM at 72 hours with the MTT assay. The treatment of cells with ferulic acid concentrations of 30 and 60 μM caused a significant increase in the apoptosis index. The Bcl-2 gene expression level was significantly lower in the treated group than in the control group, and the Bax gene expression level was significantly higher in the treated group than in the control group (P < 0.001). Conclusions: The results of this study showed the apoptotic activity of ferulic acid against ACHN cells. These results can be helpful in the better understanding of the anticancer mechanism of ferulic acid, suggesting this substance as an alternative drug or in combination with conventional chemical treatments for cancer treatment.

Toxic effect of TiO2 nanoparticles against human lung cancer cell line A549

2011 ◽  
Vol 31 (10) ◽  
pp. 1091-1095
Author(s):  
Xiao-lin LI ◽  
Yan-fang ZHANG ◽  
Kai TANG ◽  
Ying TANG ◽  
Ruo-bing JIN ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Toxic Effect ◽  
Cell Line ◽  
Cancer Cell ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Human Lung Cancer Cell

Characterization of the Eugenol Effects on the Bioenergetic Profile of SCC-4 Human Squamous Cell Carcinoma Cell Line

2018 ◽  
Vol 69 (9) ◽  
pp. 2567-2570 ◽  
Author(s):  
Oana M. Duicu ◽  
Ioana Z. Pavel ◽  
Florin Borcan ◽  
Danina M. Muntean ◽  
Adelina Cheveresan ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Squamous Cell ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Squamous Cell Carcinoma Cell ◽  
Human Squamous Cell Carcinoma ◽  
Extracellular Flux ◽  
Transport Chain

Eugenol (EU), the active ingredient in clove oil, is commonly used as successful therapeutic compound in dentistry due to its antiseptic and anti-inflammatory effects. Recent research studies suggest that eugenol has also a potential anti-cancer effect. This study was thereby purported to assess the effects of EU on the bioenergetic profile of the SCC-4 human squamous cell carcinoma cell line. To this aim, SCC-4 cells were treated for 24 hours with free EU and EU incorporated in polyurethane structures (50 �M each). Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were measured using the Seahorse XF-24e extracellular flux analyzer (Agilent Technologies Inc.). Analysis of the SCC-4 bioenergetic profile was performed in the presence of the classic modulators of the electron transport chain: oligomycin, FCCP, and antimycin A+rotenone. Our data showed that cells stimulated with free EU induced a decrease of OCR linked parameters and an increase of ECAR, effects that were abolished by the incorporation of EU in polyurethane structures. In conclusion, free eugenol elicits inhibitory effects on mitochondrial respiration in the SCC-4 cell line, a result that might be suggestive for its anti-tumoral effects.

scholarly journals Reciprocal transactivation of Merkel cell polyomavirus and high-risk human papillomavirus promoter activities and increased expression of their oncoproteins

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Kashif Rasheed ◽  
Baldur Sveinbjørnsson ◽  
Ugo Moens
Keyword(s):  
High Risk ◽  
Cell Carcinoma ◽  
Cell Line ◽  
Merkel Cell Carcinoma ◽  
Transcriptional Activity ◽  
Carcinoma Cell ◽  
Merkel Cell ◽  
Late Promoter ◽  
Tumor Viruses ◽  
E6 And E7

Abstract Background Approximately 15% of human cancers are attributed to viruses. Numerous studies have shown that high-risk human polyomaviruses (HR-HPV) and Merkel cell polyomavirus (MCPyV) are two human tumor viruses associated with anogenetal and oropharyngeal cancers, and with Merkel cell carcinoma, respectively. MCPyV has been found in HR-HPV positive anogenetal and oropharyngeal tumors, suggesting that MCPyV can act as a co-factor in HR-HPV induced oncogenesis. This prompted us to investigate whether the oncoproteins large T-antigen (LT) and small antigen (sT) of MCPyV could affect the transcriptional activity HPV16 and HPV18 and vice versa whether HPV16 and HPV18 E6 and E7 oncoproteins affected the expression of MCPyV LT and sT. Reciprocal stimulation of these viral oncoproteinscould enhance the oncogenic processes triggered by these tumor viruses. Methods Transient co-transfection studies using a luciferase reporter plasmid with the long control region of HPV16 or HPV18, or the early or late promoter of MCPyV and expression plasmids for LT and sT, or E6 and E7, respectively were performed in the HPV-negative cervical cancer cell line C33A, in the keratinocyte cell line HaCaT, and in the oral squamous cell carcinoma cell line HSC-3. Transfections were also performed with deletion mutants of all these promoters and with mutants of all four oncoproteins. Finally, the effect of E6 and E7 on LT and sT expression in the MCPyV-positive Merkel cell carcinoma cell line WaGa and the effect of LT and sT on the expression of E6 and E7 was monitored by Western blotting. Results LT and sT stimulated the transcriptional activity of the HPV16 and HPV18 LCR and v.v. E6 and E7 potentiated the MCPyV early and late promoter in all cell lines. Induction by E6 and E7 was p53- and pRb-independent, and transactivation by LT did not require DNA binding, nuclear localization and HSC70/pRb interaction, whereas sT stimulated the HPV16/18 LCR activity in a PP2A- and DnaJ-independent manner. Conclusions These results indicate that the co-infection of MCPyV may act as a co-factor in the initiation and/or progression of HPV-induced cancers.

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