scholarly journals Tilianin Extracted From Dracocephalum moldavica L. Induces Intrinsic Apoptosis and Drives Inflammatory Microenvironment Response on Pharyngeal Squamous Carcinoma Cells via Regulating TLR4 Signaling Pathways

2020 ◽  
Vol 11 ◽  
Author(s):  
Hailun Jiang ◽  
Li Zeng ◽  
Xueqi Dong ◽  
Shuilong Guo ◽  
Jianguo Xing ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Intrinsic Apoptosis ◽  
Tlr4 Signaling ◽  
Inflammatory Microenvironment ◽  
Squamous Carcinoma Cells

scholarly journals Furano-1,2-Naphthoquinone Inhibits Src and PI3K/Akt Signaling Pathways in Ca9-22 Human Oral Squamous Carcinoma Cells

2012 ◽  
Vol 13 (3) ◽  
pp. NP18-NP28 ◽  
Author(s):  
Kuei-Li Lin ◽  
Ching-Ming Chien ◽  
Chih-Hua Tseng ◽  
Yeh-Long Chen ◽  
Long-Sen Chang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Squamous Carcinoma ◽  
Akt Signaling ◽  
Carcinoma Cells ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma

scholarly journals α-Lipoic Acid Induces Intrinsic Apoptosis in Human Oral Squamous Carcinoma Cells

2021 ◽  
Author(s):  
Revathi Duraisamy ◽  
Ezhilarasan Devaraj ◽  
Elumalai Perumal
Keyword(s):  
Gene Expression ◽  
Lipoic Acid ◽  
Squamous Carcinoma ◽  
Carcinoma Cells ◽  
Oxygen Species ◽  
Intrinsic Apoptosis ◽  
Apoptotic Gene ◽  
Squamous Carcinoma Cells ◽  
Oral Squamous Carcinoma ◽  
Dual Staining

Abstract Oral squamous cell carcinoma is one of the leading cancers in India and it is responsible for significant morbidity and mortality. α -lipoic acid, a co-factor for several metabolic enzymes, suppresses the tumor growth. In this study, we investigated the α-lipoic acid-induced cytotoxicity and apoptosis in human oral squamous carcinoma (SCC-25) cells. α-lipoic acid treatments were given to SCC-25 cells for 24 h and cell proliferation was evaluated by MTT assay. The reactive oxygen species expression was examined by dichloro-dihydro-fluorescein diacetate assay. Apoptosis-related morphological changes were detected by dual staining. Cytochrome c and RAS (H-Ras) expression was measured by dual staining and RT-PCR respectively. Intrinsic apoptosis-related markers are analyzed using qPCR.α-lipoic acid inhibited SCC-25 cell proliferation in a concentration-dependent manner. This treatment also increased intracellular reactive oxygen species expression and the percentage of apoptotic cells (up to 70% of the cell population). Dual staining further confirms cytochrome c cytosolic expression. The oncogene H-Ras protein and gene expression was also down-regulated upon α-lipoic acid treatment in SCC-25 cells. qPCR analysis further confirms α-lipoic acid-induced an upregulation of bax, Apaf-1, caspase 3 and − 9, pro-apoptotic gene expressions and downregulation of bcl-2, an anti-apoptotic gene expression. The present results suggest that α-lipoic acid has cytotoxic and pro-apoptotic potential and it also downregulates H-Ras oncogene expression in human oral squamous carcinoma cells. α-lipoic acid may have promising role in the treatment of human oral squamous carcinoma.

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.

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