scholarly journals Caffeic Acid and Metformin Inhibit Invasive Phenotype Induced by TGF-β1 in C-4I and HTB-35/SiHa Human Cervical Squamous Carcinoma Cells by Acting on Different Molecular Targets

2018 ◽  
Vol 19 (1) ◽  
pp. 266 ◽  
Author(s):  
Malgorzata Tyszka-Czochara ◽  
Malgorzata Lasota ◽  
Marcin Majka
Keyword(s):  
Caffeic Acid ◽  
Molecular Targets ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Invasive Phenotype ◽  
Squamous Carcinoma Cells ◽  
Tgf Β1

TGF-β1 inhibits the growth and metastasis of tongue squamous carcinoma cells through Smad4

Gene ◽  
2011 ◽  
Vol 485 (2) ◽  
pp. 160-166 ◽  
Author(s):  
Xiumei Wang ◽  
Wenjing Sun ◽  
Chengren Zhang ◽  
Guohua Ji ◽  
Yana Ge ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells ◽  
Tongue Squamous Carcinoma ◽  
Tgf Β1

scholarly journals Induction of Cell Cycle Arrest and Apoptotic Response of Head and Neck Squamous Carcinoma Cells (Detroit 562) by Caffeic Acid and Caffeic Acid Phenethyl Ester Derivative

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Arkadiusz Dziedzic ◽  
Robert Kubina ◽  
Agata Kabała-Dzik ◽  
Marta Tanasiewicz
Keyword(s):  
Cell Cycle ◽  
Phenolic Compounds ◽  
Head And Neck ◽  
Caffeic Acid ◽  
Squamous Carcinoma ◽  
Human Head ◽  
Caffeic Acid Phenethyl Ester ◽  
Carcinoma Cells ◽  
Dead Cell ◽  
Squamous Carcinoma Cells

Natural polyphenols have been observed to possess antiproliferative properties. The effects, including apoptotic potential of bioactive phenolic compounds, caffeic acid (CA) and its derivative caffeic acid phenethyl ester (CAPE), on cell proliferation and apoptosis in human head and neck squamous carcinoma cells (HNSCC) line (Detroit 562) were investigated and compared. Cancer cells apoptosis rates and cell cycle arrests were analysed by flow cytometry. Exposure to CA and CAPE was found to result in a dose-dependent decrease in the viability of Detroit 562 cells at different levels. CA/CAPE treatment did significantly affect the viability of Detroit 562 cells (MTT results). CAPE-mediated loss of viability occurred at lower doses and was more pronounced, with the concentrations which inhibit the growth of cells by 50% estimated at 201.43 μM (CA) and 83.25 μM (CAPE). Dead Cell Assay with Annexin V labelling demonstrated that CA and CAPE treatment of Detroit 562 cells resulted in an induction of apoptosis at 50 μM and 100 μM doses. The rise of mainly late apoptosis was observed for 100 μM dose and CA/CAPE treatment did affect the distribution of cells in G0/G1 phase. A combination of different phenolic compounds, potentially with chemotherapeutics, could be considered as an anticancer drug.

scholarly journals Tumour-derived TGF-β1 modulates myofibroblast differentiation and promotes HGF/SF-dependent invasion of squamous carcinoma cells

2004 ◽  
Vol 90 (4) ◽  
pp. 822-832 ◽  
Author(s):  
M P Lewis ◽  
K A Lygoe ◽  
M L Nystrom ◽  
W P Anderson ◽  
P M Speight ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Myofibroblast Differentiation ◽  
Squamous Carcinoma Cells ◽  
Tgf Β1

scholarly journals Cytotoxic Influence of Khat (Catha edulis (Vahl) Forssk. ex Endl) on Oral Fibroblasts, Squamous Carcinoma Cells, and Expression of α Smooth Muscle Actin

2021 ◽  
Vol 11 (8) ◽  
pp. 3524
Author(s):  
Azeem Ul Yaqin Syed ◽  
Muhammad A. Ahmed ◽  
Eman I. AlSagob ◽  
Mansour Al-Askar ◽  
Abdulrahman M. AlMubarak ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Control Cell ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Muscle Actin ◽  
Catha Edulis ◽  
Squamous Carcinoma Cells ◽  
Dose Dependent

The aim was to determine the cytotoxicity of Khat (Catha edulis (Vahl) Forssk. ex Endl) on normal oral fibroblasts (NOFs) and SCC4 (squamous carcinoma cells) along with expression of α-smooth muscle actin (α-SMA) in fibroblasts. Khat filtrate was prepared to obtain a concentrated viscous solution. NOFs and SCC4 cells were cultured in biological cabinets and were grown in Dulbeccos’ modified Eagles medium. Frozen cells were thawed at 37 °C and cell seeding was performed. NOFs and SCC4 cells were seeded on 96 well plates and allowed to attach. The medium was removed and a fresh medium containing different concentrations of Khat was added. The group without Khat served as a negative control and 4% paraformaldehyde as the positive control. Cell viability was assessed using the MTT assay and effect of Khat on fibroblast and SCC4 phenotypes was evaluated by immunostaining. Analysis of variance was used to assess data (p < 0.05). NOF 316 showed cell death in response to 4% paraformaldehyde, 12.5, 6.25, and 3.12 mg/mL of Khat. The highest concentration of Khat (25 mg/mL) failed to cause cytotoxicity of NOF 316. NOF 319 and NOF 26 displayed cell death at all concentrations of Khat, however, cytotoxicity was not dose dependent. NOF 18 and SCC4 cells showed dose-dependent cell death. NOF 316 showed α-SMA expression after 1 mg/mL of Khat exposure. Not all fibroblasts were α-SMA-positive, suggesting specific activation of a subset of fibroblasts. Khat is cytotoxic to NOF and SCC4 cells. Furthermore, it can also cause activation and phenotypic changes in oral fibroblasts, indicating a potential role in progression of oral squamous cell carcinoma.

Upregulation of HO-1 is accompanied by activation of p38MAPK and mTOR in human oesophageal squamous carcinoma cells

2013 ◽  
Vol 37 (6) ◽  
pp. 584-592 ◽  
Author(s):  
Jian-Li Hu ◽  
Lan Xiao ◽  
Zhen-Yun Li ◽  
Qiong Wang ◽  
Yu Chang ◽  
...  
Keyword(s):  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells
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