We show that selective EP4 antagonists (EP4A) could mitigate all of these events tested with cells in vitro as well as in vivo in syngeneic COX-2 expressing mammary cancer bearing mice or immune-deficient mice bearing COX-2 over-expressing human breast cancer xenografts.
However, the functional aspects of EP3 receptor in breast cancer and the way how EP3 may oppose the pro-tumorigenic effects of PGE2 elevation and COX-2 overexpression are not fully understood so far.
Our findings suggest that concurrent use of glucocorticoids, ACE inhibitors, aspirin, NSAIDs, selective COX-2 inhibitors, digoxin, and opioids has little impact on breast cancer recurrence.
MiR655 expression positively correlated with COX-2 in genetically disparate breast cancer cell lines and increased in all cell lines when grown as spheroids, implicating its link with stem-like cells (SLCs).
All these experiments suggest that ME inhibits breast cancer cell proliferation and apoptosis by inhibiting the expression of COX-2 in MCF-7 and MDAMB- 468 cells.
In conclusion, rcdtB treatment inhibited tumor growth and induced apoptosis through inhibiting Bcl-2 expression, inflammatory responses, and activating C-erbB-2 and Cox-2 expression in breast cancer mouse model.
Analysis of clinical samples demonstrated that COX-2/PGE<sub>2</sub> /EP<sub>4</sub> signaling is elevated in basal-like and chemoresistant breast carcinoma and is correlated with survival and relapse of breast cancer.
Here, we evaluate the impact of the four most common cyclooxygenase-2 gene polymorphisms (rs689465, rs689466, rs20417 and rs20417), in combination with obesity, on the risk of breast cancer progression in a cohort of Brazilian breast cancer patients (<i>N</i> = 1038).
The results of the present study revealed that HPV16 E7 may promote the proliferation of breast cancer cells by upregulating COX-2, suggesting that COX-2 may be a potential therapeutic target for HPV16 E7-mediated progression of breast cancer.
Further study suggested that AKT1 and cyclooxygenase-2 (COX2; PTGS2) might mediate the CXCR2 signaling to inversely control the breast cancer metastasis and chemoresistance through the regulation of EMT, apoptosis, and senescence.
This work demonstrated the potential anti-cancer effects of Andro, indicating that Andro could inhibit COX-2 expression through attenuating p300 HAT activity and suppress angiogenesis via VEGF pathway, and thereby could be developed as an antitumor agent for the treatment of breast cancer.
Bioinformatics analysis revealed that COX-2 is highly expressed in TNBC and that its expression correlated with poor survival outcome in basal subtype of breast cancer.
By using Spearman correlation analysis, the correlations between expression of PCNA, Ki-67 and COX-2 and X-ray features in mammography in breast cancer were investigated.
The present findings demonstrated that EpCAM was involved in the regulation of COX‑2 expression, and a positive correlation between the proteins was associated with poor prognosis in patients with breast cancer.
We also demonstrate that cigarette smoke induces the expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 and reduces 15-hydroxyprostaglandin dehydrogenase, resulting in prostaglandin E<sub>2</sub> release in human breast cancer.
Higher COX-2 expression was associated with lower risk for breast cancer events during the first five years of follow-up, <sub>adj</sub> HR 0.60 (95%CI: 0.37-0.97), per category.
BPA induced COX-2 expression via nuclear translocation of NF-κB and activation of mitogen-activated protein kinase (MAPK) by phosphorylation of ERK1/2 and enhanced the migration of lung cancer A549 and breast cancer MDAMB-231 cells.