2013
DOI: 10.3892/or.2013.2549
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Cyclooxygenase-2 utilizes Jun N-terminal kinases to induce invasion, but not tamoxifen resistance, in MCF-7 breast cancer cells

Abstract: Abstract. Elevated cyclooxygenase-2 (COX-2) expression in breast tumors is associated with a lower survival rate in patients with estrogen receptor α (ERα)-positive tumors. We hypothesized that COX-2 reduces the survival rate of breast cancer patients with ERα-positive tumors since COX-2 increases the invasiveness of ERα-positive breast tumors and decreases tumor sensitivity to tamoxifen. Previously, we demonstrated that COX-2 stimulates the activity of protein kinase C (PKC) to increase the invasiveness of ER… Show more

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Cited by 11 publications
(7 citation statements)
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“…Jun is activated through phosphorylation at Ser 63 and Ser 73 by JNK [92,93]. A high level of Jun has been observed in various types of cancer including non-small cell lung cancer, oral squamous cell carcinoma, breast cancer and colorectal cancer [94,95,96,97,98]. Overexpression of Jun has led to aberrant tumor growth and progression and inhibited cell apoptosis [94].…”
Section: Resultsmentioning
confidence: 99%
“…Jun is activated through phosphorylation at Ser 63 and Ser 73 by JNK [92,93]. A high level of Jun has been observed in various types of cancer including non-small cell lung cancer, oral squamous cell carcinoma, breast cancer and colorectal cancer [94,95,96,97,98]. Overexpression of Jun has led to aberrant tumor growth and progression and inhibited cell apoptosis [94].…”
Section: Resultsmentioning
confidence: 99%
“…However, there also existed an experiment identified that this function did not perform effects. They found that Cox‐2 stimulated the activity of protein kinase C ( PKC ) to enhance the phosphorylation of Jun N‐terminal kinases ( JNKs ), but not that of AKT family members in estrogen receptor ( ER ) positive cells [29]. This difference might due to the different microenvironments between various cells.…”
Section: Discussionmentioning
confidence: 99%
“…4 × 105 cells were pretreated with the JNK inhibitor SP600125 (0, 5 or 10 μM) in RPMI 1640 medium containing 5% FBS for 30 min before being added to the Matrigel-coated Transwell inserts. The cells, migrated for 12 h, were fixed and counted in 10 high-powered (×200) fields under a microscope as mentioned by Gonzalez-Villasana V et al [22]. The experiment was repeated three times.…”
Section: Methodsmentioning
confidence: 99%