scholarly journals Syringic acid modulates molecular marker–involved cell proliferation, survival, apoptosis, inflammation, and angiogenesis in DMBA‐induced oral squamous cell carcinoma in Syrian hamsters

2020 ◽  
Vol 34 (11) ◽  
Author(s):  
Velu Periyannan ◽  
Vijayalakshmi Annamalai ◽  
Vinothkumar Veerasamy
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Molecular Marker ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Syringic Acid ◽  
Syrian Hamsters

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.

scholarly journals Knockdown of circ_0011946 targets miR-216a-5p/BCL2L2 axis to regulate proliferation, migration, invasion and apoptosis of oral squamous cell carcinoma cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Zhou ◽  
Shuhong Zhang ◽  
Zhonghan Min ◽  
Zhongwei Yu ◽  
Huaiwei Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
B Cell Lymphoma ◽  
Luciferase Reporter ◽  
Migration And Invasion

Abstract Background Circular RNAs (circRNAs) are implicated in the development of oral squamous cell carcinoma (OSCC). The aim of current research is to elucidate the role and mechanism of circ_0011946 in the functional behaviors of OSCC cells. Methods Circ_0011946, microRNA (miR)-216a-5p, B cell lymphoma-2-like 2 protein (BCL2L2) abundances were exposed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation, migration, invasion and apoptosis were detected by MTT, colony formation assay, transwell, wound-healing and flow cytometry assays, respectively. Target correlation was tested by dual-luciferase reporter and RNA pull-down assays. An in vivo xenograft experiment was employed to investigate the function of circ_0011946 on tumor growth in vivo. Results Circ_0011946 and BCL2L2 levels were increased, while miR-216a-5p level was decreased in OSCC tissues and cells. Circ_0011946 knockdown impeded proliferation, migration, and invasion, but promoted apoptosis in OSCC cells. Circ_0011946 functioned as a sponge for miR-216a-5p, and BCL2L2 was targeted by miR-216a-5p. Besides, miR-216a-5p or BCL2L2 knockdown partly attenuated the inhibitory influences of circ_0011946 silence or miR-216a-5p overexpression on OSCC cell progression. Furthermore, circ_0011946 post-transcriptionally regulated BCL2L2 through sponging miR-216a-5p. Moreover, circ_0011946 knockdown constrained OSCC tumor growth in vivo. Conclusion Circ_0011946 silence repressed OSCC cell proliferation, migration, and invasion, but promoted apoptosis through the regulation of the miR-216a-5p/BCL2L2 axis.

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