scholarly journals Demethylation restores SN38 sensitivity in cells with acquired resistance to SN38 derived from human cervical squamous cancer cells

2012 ◽  
Vol 27 (4) ◽  
pp. 1292-1298 ◽  
Author(s):  
TETSUJI TANAKA ◽  
TAO BAI ◽  
SAORI TOUJIMA ◽  
TOMOKO UTSUNOMIYA ◽  
TOSHIHIDE MATSUOKA ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Acquired Resistance ◽  
Squamous Cancer ◽  
Cervical Squamous Cancer ◽  
In Cells

scholarly journals Immune negative regulator TIPE2 inhibits cervical squamous cancer progression through Erk1/2 signaling

2019 ◽  
Vol 14 (1) ◽  
pp. 528-536
Author(s):  
Li-Qiong Huang ◽  
Bo Zheng ◽  
Yi He
Keyword(s):  
Cervical Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Erk Signaling ◽  
Over Expression ◽  
Squamous Cancer ◽  
Cancer Tissues ◽  
Proliferation And Invasion ◽  
Cervical Squamous Cancer

AbstractTumor necrosis factor (TNF)-α-induced protein-8-like 2, or TIPE2, is a newly found immune negative regulatory molecule. This study further investigated the role of TIPE2 on proliferation and invasion of cervical squamous cancer cells. Expression of TIPE2 was compared in cervical squamous cancer tissues and adjacent normal tissues by Western blot and immunohistochemistry (IHC). Cervical squamous cancer cell lines, SiHa and C33A, were transfected with recombinant plasmid encoding TIPE2 and tested for cytologic characteristics. The impact of TIPE2 on phosphorylation of extracellular signal-regulated kinase (Erk) signaling pathway was also tested by Western blot analysis of key factors. TIPE2 expression was higher in cervical cancer tissues than that in normal tissue. IHC score of tumor tissue was negatively associated with lymphatic metastasis. Over expression of TIPE2 effectively inhibited the proliferation of cervical cancer cells. Wound healing and transwell assay showed that over expression of TIPE2 suppressed cell migration and invasion in vitro. Meanwhile, phosphorylation of Erk1/2 and upstream mitogen-activated protein kinase kinase (MEK) 1/2 was reduced by TIPE2. TIPE2 is negatively related with development of cervical squamous cancer. TIPE2 is an inhibitory factor of proliferation and invasion of cervical squamous cancer cells, probably through inhibiting Erk signaling pathway.

scholarly journals AGER promotes proliferation and migration in cervical cancer

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Xuejie Zhu ◽  
Lulu Zhou ◽  
Ruyi Li ◽  
Qi Shen ◽  
Huihui Cheng ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Tumor Promoter ◽  
Biological Behavior ◽  
Squamous Cervical Cancer ◽  
Glycation End Products ◽  
Squamous Cancer ◽  
And Migration ◽  
Cervical Squamous Cancer

The receptor for advanced glycation end products (AGER) is an oncogenic transmembranous receptor up-regulated in various human cancers. We have previously reported that AGER was overexpressed in squamous cervical cancer. However, mechanisms of AGER involved in the progression of cervical cancer are unknown. In the present study, we investigated the effects of AGER on biological behavior, including proliferation, apoptosis, and migration using multiple biological approaches. AGER protein primarily localized in the cytoplasm and cytomembrane of cervical squamous cancer cells. Blockage of AGER with multiple siRNAs suppressed proliferation, stimulated apoptosis, inhibited migration of cervical squamous cancer cells. Conversely, overexpression of AGER increased cell proliferation, migration, and inhibited cell apoptosis. These results indicate that AGER promotes proliferation, migration, and inhibits apoptosis of squamous cervical cancer and might function as a tumor promoter in cervical cancer. Our study provides novel evidence for a potential role of AGER in bridging human papillomavirus (HPV)-induced inflammation and cervical cancer.

scholarly journals RasOncogene-Mediated Progressive Silencing of Extracellular Superoxide Dismutase in Tumorigenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Francesca Cammarota ◽  
Gabriella de Vita ◽  
Marco Salvatore ◽  
Mikko O. Laukkanen
Keyword(s):  
Superoxide Dismutase ◽  
Cancer Cells ◽  
Self Regulation ◽  
Thyroid Cell ◽  
Extracellular Superoxide Dismutase ◽  
Mrna Synthesis ◽  
Ras Activation ◽  
Degree Of Differentiation ◽  
In Cells

Extracellular superoxide dismutase (SOD3) is a secreted enzyme that uses superoxide anion as a substrate in a dismutase reaction that results in the formation of hydrogen peroxide. Both of these reactive oxygen species affect growth signaling in cells. Although SOD3 has growth-supporting characteristics, the expression ofSOD3is downregulated in epithelial cancer cells. In the current work, we studied the mechanisms regulatingSOD3expressionin vitrousing thyroid cell models representing different stages of thyroid cancer. We demonstrate that a low level of RAS activation increasesSOD3mRNA synthesis that then gradually decreases with increasing levels of RAS activation and the decreasing degree of differentiation of the cancer cells. Our data indicate thatSOD3regulation can be divided into two classes. The first class involves RAS–driven reversible regulation ofSOD3expression that can be mediated by the following mechanisms: RAS GTPase regulatory genes that are responsible forSOD3self-regulation; RAS-stimulated p38 MAPK activation; and RAS-activated increased expression of themir21microRNA, which inversely correlates withsod3mRNA expression. The second class involves permanent silencing ofSOD3mediated by epigenetic DNA methylation in cells that represent more advanced cancers. Therefore, the work suggests thatSOD3belongs to the group ofrasoncogene-silenced genes.

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