scholarly journals LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression

2017 ◽  
Vol 6 (12) ◽  
pp. 2897-2908 ◽  
Author(s):  
Zheng Fang ◽  
Junfang Zhao ◽  
Weihong Xie ◽  
Qiang Sun ◽  
Haibin Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cisplatin Resistance

scholarly journals LncRNA PVT1 Enhances Proliferation and Cisplatin Resistance via Regulating miR-194-5p/HIF1a Axis in Oral Squamous Cell Carcinoma

2020 ◽  
Vol Volume 13 ◽  
pp. 243-252 ◽  
Author(s):  
Fang Wang ◽  
Xin Ji ◽  
Jingjing Wang ◽  
Xiangrui Ma ◽  
Yong Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cisplatin Resistance

scholarly journals Overexpression ofβ-Catenin Induces Cisplatin Resistance in Oral Squamous Cell Carcinoma

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Long Li ◽  
Hai-Chao Liu ◽  
Cheng Wang ◽  
Xiqiang Liu ◽  
Feng-Chun Hu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Cisplatin Resistance ◽  
Stable Cell Lines ◽  
Abnormal Expression

Abnormal expression ofβ-catenin contributes to tumor development, progression, and metastasis in various cancers. However, little is known about the relationship between abnormal expression ofβ-catenin and cisplatin chemotherapy in oral squamous cell carcinoma (OSCC). The present study aimed to investigate the effect ofβ-catenin on OSCC cisplatin resistance and evaluated the drug susceptibility of stable cell lines withβ-catenin knockin and knockdown. In this study, we found that higher expression level ofβ-catenin can be observed in CDDP-treated cell lines as compared with the control group. Furthermore, the expression levels ofβ-catenin increased in both a concentration- and time-dependent manner with the cisplatin treatment. More importantly, the nuclear translocation ofβ-catenin could also be observed by confocal microscope analysis. Stable cell lines with CTNNB1 knockin and knockdown were established to further investigate the potential role and mechanism ofβ-catenin in the chemoresistance of OSCC in vitro and in vivo. Our findings indicated that overexpression ofβ-catenin promoted cisplatin resistance in OSCC in vitro and in vivo. We confirmed that GSK-3β, C-myc, Bcl-2, P-gp, and MRP-1 were involved inβ-catenin-mediated drug resistance. Our findings indicate that the Wnt/β-catenin signaling pathway may play important roles in cisplatin resistance in OSCC.

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