scholarly journals Syringic acid suppresses oral squamous cell carcinoma SCC131 cell proliferation via modulation of mitochondria‐mediated apoptosis signaling pathways

2020 ◽  
Vol 34 (12) ◽  
Author(s):  
Periyannan Velu ◽  
Annamalai Vijayalakshmi ◽  
Veerasamy Vinothkumar
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Squamous Cell ◽  
Syringic Acid

scholarly journals Inhibition of Cell Proliferation and MAP Kinase and Akt Pathways in Oral Squamous Cell Carcinoma by Genistein and Biochanin A

2010 ◽  
Vol 7 (3) ◽  
pp. 351-358 ◽  
Author(s):  
Tara L. Johnson ◽  
Maria B. Lai ◽  
James C. K. Lai ◽  
Alok Bhushan
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Cancer ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Squamous Cell ◽  
Biochanin A ◽  
High Morbidity

High morbidity and mortality associated with oral squamous cell carcinoma (OSCC) are largely attributable to late stage diagnosis. Despite significant advances in therapeutic strategies, the five-year survival rate for oral cancer remains at about 50%. A chemopreventive approach may be an effective alternative or adjunct to current therapies. Previous studies have shown anti-tumor effects of isoflavones in several cancers, including oral cancer. However, their mechanisms of action are still unclear. We hypothesized that isoflavones inhibit multiple signaling pathways implicated in oral carcinogenesis. To address our hypothesis, we investigated the effects of three isoflavone derivatives, genistein, biochanin A and daidzein, on SCC15 and SCC25 squamous cell carcinoma cell lines. In cell proliferation experiments, we found that genistein and biochanin A inhibited SCC15 and SCC25 cell growth with an IC50 of 50 μM. We also investigated the effect of isoflavones on ERK and Akt pathways. Our results, from western blot analysis, suggest that both genistein and biochanin A induced decreases in phosphorylation of ERK and Akt at treatment concentrations of 20, 50 and 100 μM. Taken together, our results clearly demonstrate a differential regulation of signaling pathways by various isoflavones in OSCC cell lines. Thus, tumor progression models can be utilized to study the preventive and therapeutic roles of isoflavones in oral cancer cell lines.

scholarly journals Licochalcone B induces apoptosis of human oral squamous cell carcinoma through the extrinsic- and intrinsic-signaling pathways

2016 ◽  
Vol 48 (4) ◽  
pp. 1749-1757 ◽  
Author(s):  
HANA OH ◽  
GOO YOON ◽  
JAE-CHEON SHIN ◽  
SEON-MIN PARK ◽  
SEUNG-SIK CHO ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Squamous Cell

scholarly journals Analysis of cell proliferation and pattern of invasion in oral squamous cell carcinoma

2010 ◽  
Vol 52 (3) ◽  
pp. 417-424 ◽  
Author(s):  
Satiro Watanabe ◽  
Rogério Watanabe ◽  
Angélica F. Oton-Leite ◽  
Rita de C. G. Alencar ◽  
José C. Oliveira ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Pattern Of Invasion

Bone Marrow Mesenchymal Stem Cells (BMSCs) with High Expression miR-155 Affect the Proliferation and Metastasis of Oral Squamous Cell Carcinoma by Regulating Phosphatase and Tensin Homolog 12 (PTEN12)

2021 ◽  
Vol 11 (8) ◽  
pp. 1571-1575
Author(s):  
Guowu Ma ◽  
Jia Hou ◽  
Jiezi Qiu ◽  
Jianlin Fan ◽  
Jianxin Yang
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
High Expression ◽  
Tensin Homolog ◽  
Proliferation And Metastasis ◽  
Apoptotic Activity ◽  
And Migration

Oral squamous cell carcinoma (OSCC) had the poor prognosis. miR-155 was involved in some diseases. However, whether BMSCs with high expression miR-155 affect the proliferation and metastasis of OSCC is unclear. Our study aims to assess BMSCs’ effect on OSCC cells. miR-155 level in OSCC tumor tissues was analyzed. BMSCs were transfected with miR-155 followed by analysis of cell proliferation by MTT assay, cell apoptosis and migration, and MMP-9 level by ELISA and PTEN12 level. In the tumor tissue, miR-155 level was significantly increased (P <0.05). Co-culture of BMSCs with high expression miR-155 with OSCC cells could significantly promote OSCC cell proliferation and reduced cell apoptotic activity, increased cell migration and MMP-9 secretion as well as downregualted PTEN12 expression (P <0.05). In conclusion, miR-155 was increased in the OSCC patients and BMSCs of high expression miR-155 could promote the proliferation and metastasis of OSCC by regulating PTEN12.

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