Activation of G-protein coupled estrogen receptor inhibits the proliferation of cervical cancer cells via sustained activation of ERK1/2

2015 ◽  
Vol 33 (3) ◽  
pp. 134-142 ◽  
Author(s):  
Qiong Zhang ◽  
Yuan-Zhe Wu ◽  
Yan-Mei Zhang ◽  
Xiao-Hong Ji ◽  
Qun Hao
Keyword(s):  
Cervical Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
G Protein ◽  
Cervical Cancer Cells ◽  
G Protein Coupled ◽  
Sustained Activation

scholarly journals MicroRNA-300 Inhibits the Proliferation and Metastasis of Cervical Cancer Cells via Posttranscriptional Suppression of G Protein-Coupled Receptor 34 (GPR34)

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Mei Wang ◽  
Ying Tian ◽  
Lin Miao ◽  
Wenxia Zhao
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
G Protein ◽  
Migration And Invasion ◽  
G Protein Coupled Receptor ◽  
Gynecological Disorders ◽  
Cervical Cancer Cells ◽  
G Protein Coupled

Cervical cancer is one of the dominant gynecological disorders which has poor prognosis and often diagnosed at advanced stages where it becomes nearly impossible to effectively manage this disorder. MicroRNA-300 (miR-300) has dual role in human tumorogenesis. However, characterization of its regulatory action has not been made in cervical cancer. The molecular role of miR-300 in cervical cancer was thus explored in the present study with prime focus on elucidating its mechanism of action. The results showed significant (P < 0.05) downregulation of miR-300 in cervical cancer. Overexpression of miR-300 in cervical cancer cells inhibited their proliferation in vitro by inducing apoptosis. Cervical cancer cells overexpressing miR-300 also showed decreased rates of migration and invasion. G protein-coupled receptor 34 (GPR34) was found to be the functional regulatory target of miR-300 in cervical cancer. GPR34 was found to be significantly (P < 0.05) overexpressed in cervical cancer tissues and cell lines. Silencing of GPR34 inhibited the growth of the cervical cancer cells. However, overexpression of GPR34 could prevent the tumor-suppressive effects of miR-300 on cervical cancer cells. Collectively, the results of the current study are indicative of the tumor-suppressive regulatory role of miR-300 in cervical cancer and suggestive of the potential therapeutic value of miR-300/GPR34 molecular axis.

scholarly journals Lysine-specific histone demethylase 1A (LSD1) in cervical cancer

2020 ◽  
Vol 146 (11) ◽  
pp. 2843-2850
Author(s):  
Daniel Beilner ◽  
Christina Kuhn ◽  
Bernd P. Kost ◽  
Julia Jückstock ◽  
Doris Mayr ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Negative Correlation ◽  
Combined Therapy ◽  
Histone Demethylase ◽  
Epigenetic Changes ◽  
Cervical Cancer Cells ◽  
G Protein Coupled

Abstract Purpose Demethylation of DNA through enzymes like LSD1 showed a crucial impact on different kind of cancers. Epigenetic modifications in cervical cancer are still not fully investigated nevertheless of high interest for a therapeutic use. Methods Tumor samples of 250 cervical cancer patients were immunochemically stained and evaluated based on Immunoreactive Score. Results were statistically analyzed for clinical and pathological parameters. Results Our patient collective showed a disadvantage for 10-year survival for patients with a strong expression of LSD1 in the cytoplasm of cervical cancer cells. The results of the correlational analysis further revealed a negative correlation of LSD1 to G-protein coupled estrogen receptor (GPER). Conclusions Epigenetic changes through enzymes like LSD1 may also be of interest for patients with cervical cancer. A combined therapy with other proteins relayed to cervical cancer like GPER might be of interest for future investigations.

scholarly journals Genistein Promotes Proliferation of Human Cervical Cancer Cells Through Estrogen Receptor-Mediated PI3K/Akt-NF-κB Pathway

2018 ◽  
Vol 9 (2) ◽  
pp. 288-295 ◽  
Author(s):  
Hai-Hong Chen ◽  
Shu-Ping Chen ◽  
Qiu-Ling Zheng ◽  
Shao-Ping Nie ◽  
Wen-Juan Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer

scholarly journals GPER1 Silencing Suppresses the Proliferation, Migration, and Invasion of Gastric Cancer Cells by Inhibiting PI3K/AKT–Mediated EMT

2020 ◽  
Vol 8 ◽  
Author(s):  
En Xu ◽  
Xuefeng Xia ◽  
Chaoyu Jiang ◽  
Zijian Li ◽  
Zhi Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
G Protein ◽  
Cancer Metastasis ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
G Protein Coupled

G protein coupled estrogen receptor (GPER1) is a membrane estrogen receptor, belonging to the seven-transmembrane G protein-coupled receptors family, and has important biological functions in cancer. However, the functional role of GPER1 in gastric cancer (GC) remain incompletely understood. In the present study, we employed gene set enrichment analysis and discovered that GPER1 expression was concomitant with EMT process and was positively correlated with activation of the PI3K/AKT pathway in GC. Knockdown of GPER1 with siRNA suppressed the proliferation, migration, and invasion of AGS and MGC-803 GC cells. Knockdown of GPER1 also downregulated the mesenchymal markers N-cadherin and vimentin, upregulated E-cadherin, an epithelial marker, and suppressed expression of the Snail, Slug and Twist1 transcription factors, indicating that knockdown of GPER1 inhibited EMT. Moreover, 740Y-P, a PI3K activator, reversed the effects of GPER1 knockdown on EMT processes. Overexpression of GPER1 with plasmid can further prove these findings. In summary, these data demonstrate that GPER1 inhibition suppresses the proliferation, migration, and invasion of gastric cancer cells by inhibiting PI3K/AKT-mediated EMT. Our study elucidated the function of GPER1 in gastric cancer, and we identified PI3K/AKT-mediated EMT as a novel mechanism by which GPER1 contributes to proliferation, migration, and invasion of gastric cancer. These data suggest that combining inhibition of GPER1 and PI3K may be a potential therapeutic approach to inhibit gastric cancer metastasis.

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