scholarly journals Endocrine disrupting chemicals promote the growth of ovarian cancer cells via the ER-CXCL12-CXCR4 signaling axis

2012 ◽  
Vol 52 (9) ◽  
pp. 715-725 ◽  
Author(s):  
Julie M. Hall ◽  
Kenneth S. Korach
2012 ◽  
Vol 24 (1) ◽  
pp. 188
Author(s):  
K.-A Hwang ◽  
S.-H. Hyun ◽  
E.-B. Jeung ◽  
K.-C. Choi

Because endocrine disrupting chemicals may interfere with the endocrine systems of our body and have an oestrogenic activity, we evaluated the effects of bisphenol A (BPA) on the transcriptional levels of altered genes in oestrogen receptor (ER)-positive BG-1 ovarian cancer cells. A microarray and RT-qPCR were employed to detect gene alterations in these cells following treatments. In this study, treatment with 17-β-oestradiol (E2) or BPA increased mRNA levels of E2-responsive genes related to apoptosis, cancer and cell cycle, signal transduction and nucleic acid binding and so on. Parallel with the microarray data, the mRNA levels of some altered genes including RAB31_member RAS oncogene family (U59877), cyclin D1 (X59798), cyclin-dependent kinase 4 (U37022), IGF-binding protein 4 (U20982) and anti-mullerian hormone (NM_000479) were significantly induced by E2 or BPA in this cell model. These results indicate that BPA in parallel with E2 induced the transcriptional levels of E2-responsive genes in an ER-positive BG-1 cells. In conclusion, these microarray and RT-qPCR results indicate that BPA, a potential weak oestrogen, may have an oestrogenic effect by regulating E2-responsive genes in ER-positive BG-1 cells and that BG-1 cells would be the best in vitro model to detect these oestrogenic endocrine disrupting chemicals. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2011-0015385).


Oncogenesis ◽  
2021 ◽  
Vol 10 (7) ◽  
Author(s):  
Shuting Huang ◽  
Suiying Liang ◽  
Guandi Chen ◽  
Jing Chen ◽  
Keli You ◽  
...  

AbstractIt has been reported that chemotherapy resistance mainly contributed to treatment failure and poor survival in patients with ovarian cancer. Therefore, clarifying the molecular mechanism and identifying effective strategies to overcome drug resistance may play an important clinical impact on this malignant tumor. In our study, we found that the expression of Glycosyltransferase 8 domain containing 2 (GLT8D2) was significantly upregulated in ovarian cancer samples with CDDP (Cis-dichlorodiammine-platinum) resistance. Biological experiment demonstrate that GLT8D2 overexpression confers CDDP resistance on ovarian cancer cells; however, inhibition of GLT8D2 sensitized ovarian cancer cell lines to CDDP cytotoxicity both in vitro and in vivo. By using affinity purification/mass spectrometry (IP/MS) and reciprocal co-immunoprecipitation (co-IP) analyses, we found that GLT8D2 interacts with fibroblast growth factor receptor 1(FGFR1) in ovarian cancer cells. Furthermore, overexpression of GLT8D2 activated FGFR/PI3K signaling axis and upregulated the phosphorylation levels of FRS2a and AKT (AKT serine/threonine kinase). Importantly, pharmacological inhibition of FGFR and PI3K (phosphatidylinositol 3-kinase) signaling pathway significantly counteracted GLT8D2-induced chemoresistance and enhanced platinum’s therapeutic efficacy in ovarian cancer. Therefore, our findings suggest that GLT8D2 is a potential therapeutic target for the treatment of ovarian cancer; targeting GLT8D2/FGFR/PI3K/AKT signaling axis may represent a promising strategy to enhance platinum response in patients with chemoresistant ovarian cancer.


2020 ◽  
Vol 22 (3) ◽  
pp. 2545-2550
Author(s):  
Ruli Li ◽  
Jianbo Xiao ◽  
Sufan Tang ◽  
Xinjing Lin ◽  
Honglin Xu ◽  
...  

2018 ◽  
Author(s):  
F Guo ◽  
Z Yang ◽  
J Xu ◽  
J Sehouli ◽  
AE Albers ◽  
...  

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