scholarly journals LPAR5 Promotes Thyroid Carcinoma Cells Proliferation and Migration by Activating Class IA PI3K Catalytic Subunit p110β

2021 ◽  
Author(s):  
Wei‐Jun Zhao ◽  
Liu‐Lian Zhu ◽  
Wei‐Qiang Yang ◽  
Shuai‐Jun Xu ◽  
Jie Chen ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Catalytic Subunit ◽  
And Migration ◽  
Proliferation And Migration

Flavonoid Fraction of Citrus Reticulata Juice Reduces Proliferation and Migration of Anaplastic Thyroid Carcinoma Cells

2015 ◽  
Vol 67 (7) ◽  
pp. 1183-1190 ◽  
Author(s):  
Marilena Celano ◽  
Valentina Maggisano ◽  
Roberta Francesca De Rose ◽  
Stefania Bulotta ◽  
Jessica Maiuolo ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Citrus Reticulata ◽  
Flavonoid Fraction ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1

2021 ◽  
Vol 9 ◽  
Author(s):  
Yang Liu ◽  
Lida Liao ◽  
Changming An ◽  
Xiaolei Wang ◽  
Zhengjiang Li ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Theoretical Foundation ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Novel Therapy ◽  
And Migration ◽  
Therapy Strategies ◽  
Thyroid Carcinoma Cell ◽  
Proliferation And Migration

Novel therapy strategies are crucial for thyroid carcinoma treatment. It is increasingly important to clarify the mechanism of thyroid carcinoma progression. Several studies demonstrate that α-Enolase (ENO1) participates in cancer development; nevertheless, the role of ENO1 in thyroid carcinoma progression remains unclear. In the present study, we found that the expression of ENO1 was upregulated in thyroid carcinoma samples. Proliferation and migration of thyroid carcinoma cells were suppressed by depletion of ENO1; conversely, ENO1 overexpression promoted thyroid carcinoma cell growth and invasion. To elucidate the mechanisms, we found that the hypoxia-related mTOR/HIF1 pathway regulated ENO1 expression. ENO1 regulated the expression of CST1; knockdown of CST1 reversed the tumorigenicity enhanced by ENO1 overexpression. Taken together, our findings provide a theoretical foundation for thyroid carcinoma treatment.

scholarly journals Opposing function of MYBBP1A in proliferation and migration of head and neck squamous cell carcinoma cells

BMC Cancer ◽  
2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Gustavo A Acuña Sanhueza ◽  
Leonie Faller ◽  
Babitha George ◽  
Jennifer Koffler ◽  
Vinko Misetic ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
Neck Squamous Cell Carcinoma ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Erratum to: NLK is a key regulator of proliferation and migration in gallbladder carcinoma cells

2012 ◽  
Vol 368 (1-2) ◽  
pp. 217-217
Author(s):  
Zhujun Tan ◽  
Maolan Li ◽  
Wenguang Wu ◽  
Lin Zhang ◽  
Qichen Ding ◽  
...  
Keyword(s):  
Gallbladder Carcinoma ◽  
Carcinoma Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Differential roles of RET isoforms in medullary and papillary thyroid carcinomas

2017 ◽  
Vol 24 (1) ◽  
pp. 53-69 ◽  
Author(s):  
Eric Y Lian ◽  
Sarah M Maritan ◽  
Jessica G Cockburn ◽  
Katayoon Kasaian ◽  
Mathieu J F Crupi ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Survival ◽  
Tumour Progression ◽  
Carcinoma Cells ◽  
Protein Isoforms ◽  
Human Thyroid ◽  
Papillary Thyroid ◽  
Anoikis Resistance ◽  
Thyroid Carcinomas ◽  
And Migration

The RET receptor tyrosine kinase mediates cell proliferation, survival and migration in embryogenesis and is implicated in the transformation and tumour progression in multiple cancers. RET is frequently mutated and constitutively activated in familial and sporadic thyroid carcinomas. As a result of alternative splicing, RET is expressed as two protein isoforms, RET9 and RET51, which differ in their unique C-terminal amino acids. These isoforms have distinct intracellular trafficking and associated signalling complexes, but functional differences are not well defined. We used shRNA-mediated knockdown (KD) of individual RET isoforms or of total RET to evaluate their functional contributions in thyroid carcinoma cells. We showed that RET is required for cell survival in medullary (MTC) but not papillary thyroid carcinoma (PTC) cells. In PTC cells, RET depletion reduced cell migration and induced a flattened epithelial-like morphology. RET KD decreased the expression of mesenchymal markers and matrix metalloproteinases and reduced anoikis resistance and invasive potential. Further, we showed that RET51 depletion had significantly greater effects on each of these processes than RET9 depletion in both MTC and PTC cells. Finally, we showed that expression of RET, particularly RET51, was correlated with malignancy in a panel of human thyroid tumour tissues. Together, our data show that RET expression promotes a more mesenchymal phenotype with reduced cell–cell adhesion and increased invasiveness in PTC cell models, but is more important for tumour cell survival, proliferation and anoikis resistance in MTC models. Our data suggest that the RET51 isoform plays a more prominent role in mediating these processes compared to RET9.

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