scholarly journals Receptor tyrosine kinase, RON, promotes tumor progression by regulating EMT and the MAPK signaling pathway in human oral squamous cell carcinoma

2019 ◽  
Author(s):  
Sun‑Ae Kim ◽  
Kyung‑Hwa Lee ◽  
Dong Hoon Lee ◽  
Joon Kyoo Lee ◽  
Sang Chul Lim ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tyrosine Kinase ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Receptor Tyrosine Kinase ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

scholarly journals WNT1-inducible signaling pathway protein-1 contributes to tumor progression and treatment failure in oral squamous cell carcinoma

2017 ◽  
Vol 14 (2) ◽  
pp. 1719-1724 ◽  
Author(s):  
Eun Kyung Jung ◽  
Sun-Ae Kim ◽  
Tae Mi Yoon ◽  
Kyung-Hwa Lee ◽  
Hee Kyung Kim ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Treatment Failure ◽  
Tumor Progression ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell

scholarly journals Receptor tyrosine kinase amplification is predictive of distant metastasis in patients with oral squamous cell carcinoma

2017 ◽  
Vol 108 (2) ◽  
pp. 256-266 ◽  
Author(s):  
Yu Oikawa ◽  
Kei-ichi Morita ◽  
Kou Kayamori ◽  
Kousuke Tanimoto ◽  
Kei Sakamoto ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Tyrosine Kinase ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Receptor Tyrosine Kinase ◽  
Distant Metastasis

scholarly journals Angelicin Shows Antitumor Effects On The Oral Squamous Cell Carcinoma By Negatively Regulating DUSP6-Mediated cMYC-MAPK Signaling Pathway

2021 ◽  
Author(s):  
Na Liu ◽  
Qianhui Shang ◽  
Jiajia Qi ◽  
Qionghua Li ◽  
Yutong Sun ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Regulatory Mechanism ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Antitumor Effects

Abstract Background: Angelicin has been reported to have antitumor effects on many cancers. However, few studies on angelicin in oral squamous cell carcinoma (OSCC) have been performed. Methods: In this study, we performed a cell cycle and apoptosis assay, wound healing assay, and transwell assay to assess the effects of angelicin on malignant phenotypes of OSCC in vitro. To determine the potential regulatory mechanism, we conducted differentially expressed genes analysis of OSCC cells. Subsequently, nude mouse xenograft models were used to evaluate the function of angelicin and validate the regulatory mechanism in vivo. Results: The results showed that angelicin inhibited the malignant phenotype of OSCC in vitro and reduced tumor formation in vivo. Mechanistically, angelicin induced the downregulation of the significantly different gene—dual-specificity phosphatase 6 (DUSP6) and the downstream transcription factor c-MYC in the mitogen-activated protein kinase (MAPK) signaling pathway. Conclusion: Our results indicate that angelicin has antitumor effects on OSCC by negatively regulating the DUSP6-mediated cMYC-MAPK signaling pathway and is a promising antitumor drug in OSCC therapy.

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