COX-2 inhibition by celecoxib in epithelial ovarian cancer attenuates E-cadherin suppression through reduced Snail nuclear translocation

Wang, Yanping; Wang, Qu-Yuan; Li, Changhui; Li, Xuewei

doi:10.1016/j.cbi.2018.06.020

Cited by 24 publications

(16 citation statements)

References 21 publications

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“…An increase in COX-2 expression and a subsequent increase in intracellular PGE 2 levels have been reported in malignant tumor cells, and many previous studies have indicated that these factors have roles in EMT induction [111,112]. The significant roles of COX-2 and PGE 2 in EMT induction were confirmed in a study of pharmacological COX-2 inhibitors in breast and ovarian cancer cells [113,114]. In particular, COX-2 was associated with inflammatory signaling pathway activation, and it mediated intercellular communication between macrophages and tumor cells undergoing EMT [112,115].…”

Section: Lipid Metabolism In Emtmentioning

confidence: 93%

Role of Metabolic Reprogramming in Epithelial–Mesenchymal Transition (EMT)

Kang

Kim

Lee

et al. 2019

IJMS

122

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Activation of epithelial–mesenchymal transition (EMT) is thought to be an essential step for cancer metastasis. Tumor cells undergo EMT in response to a diverse range of extra- and intracellular stimulants. Recently, it was reported that metabolic shifts control EMT progression and induce tumor aggressiveness. In this review, we summarize the involvement of altered glucose, lipid, and amino acid metabolic enzyme expression and the underlying molecular mechanisms in EMT induction in tumor cells. Moreover, we propose that metabolic regulation through gene-specific or pharmacological inhibition may suppress EMT and this treatment strategy may be applied to prevent tumor progression and improve anti-tumor therapeutic efficacy. This review presents evidence for the importance of metabolic changes in tumor progression and emphasizes the need for further studies to better understand tumor metabolism.

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Section: Lipid Metabolism In Emtmentioning

confidence: 93%

Role of Metabolic Reprogramming in Epithelial–Mesenchymal Transition (EMT)

Kang

Kim

Lee

et al. 2019

IJMS

122

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“…Growing evidence proves that COX-2 is highly expressed in cancers such as skin cancer, liver cancer, and breast cancer. Some studies reported that COX-2 and its derivative prostaglandin E2 (PGE2) were highly expressed in ovarian cancer cells and might promote cancer cell proliferation and metastasis (36,82).…”

Section: Cyclooxygenase-2 (Cox-2)mentioning

confidence: 99%

Deregulation of Lipid Metabolism: The Critical Factors in Ovarian Cancer

Shen²,

et al. 2020

Front. Oncol.

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Ovarian cancer is one of the most malignant gynecological cancers around the world. In spite of multiple treatment options, the five-year survival rate is still very low. Several metabolism alterations are described as a hallmark in cancers, but alterations of lipid metabolism in ovarian cancer have been paid less attention. To explore new markers/targets for accurate diagnosis, prognosis, and therapeutic treatments based on metabolic enzyme inhibitors, here, we reviewed available literature and summarized several key metabolic enzymes in lipid metabolism of ovarian cancer. In this review, the rate limiting enzymes associated with fatty acid synthesis (FASN, ACC, ACLY, SCD), the lipid degradation related enzymes (MAGL, CPT, 5-LO, COX2), and the receptors related to lipid uptake (FABP4, CD36, LDLR), which promote the development of ovarian cancer, were analyzed and evaluated. We also focused on the review of application of current metabolic enzyme inhibitors for the treatment of ovarian cancer through which the potential therapeutic agents may be developed for ovarian cancer therapy.

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“…E-cadherin is the primary molecule that maintains the polarity and intercellular adhesion of epithelial cells. Its primary function is to form a protein complex which links to the actin cytoskeleton and prevents the metastasis and invasion of tumor cells (43). However, EMT can reduce or eliminate the expression of epithelial cell adhesion molecules and cytoskeletal components to achieve a stromal cell phenotype.…”

Section: Discussionmentioning

confidence: 99%

Diosgenin inhibits the epithelial‑mesenchymal transition initiation in osteosarcoma cells via the p38MAPK signaling pathway

Huang

Nie

Qin³

et al. 2019

Oncol Lett

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Diosgenin is an important basic raw material for the production of steroid hormone drugs. It can be isolated and purified from a variety of traditional Chinese medicines or plants. Modern molecular biological studies have shown that diosgenin inhibits various tumor cells migration and invasion ability to varying degrees in vitro and in vivo. The aim of the present study was to observe the inhibitory effects of diosgenin on the invasive and metastatic capabilities of osteosarcoma cells and to determine the association between the effects of diosgenin on the epithelial-mesenchymal transition (EMT). Wound healing and Transwell assays were used to observe the inhibitory effects of diosgenin on the invasion and migration of two osteosarcoma cell lines. Immunofluorescence was used to observe changes in transforming growth factor β1 (TGF-β1) protein expression levels in the osteosarcoma cells following drug administration. EMT-associated proteins, including TGFβ1, E-cadherin and vimentin were detected by western blotting, which demonstrated that the drug may inhibit the initiation of EMT in osteosarcoma cells. Western blot analysis of the expression of all the proteins in the mitogen-activated protein kinase (MAPK) pathway demonstrated that the drug inhibited the MAPK signaling pathway. The primary mechanism of action of diosgenin was the inhibition of the phosphorylated p38 (pP38) protein. Through a combination of inhibitors of the p38MAPK signaling pathway and detection of the downstream EMT marker protein E-cadherin by quantitative PCR, pP38 was confirmed to be a target of diosgenin in the inhibition of EMT in the osteosarcoma cells via the MAPK molecular signaling pathway. Diosgenin may exhibit utility as an auxiliary drug for the clinical reduction of metastasis in patients with osteosarcoma.

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COX-2 inhibition by celecoxib in epithelial ovarian cancer attenuates E-cadherin suppression through reduced Snail nuclear translocation

Cited by 24 publications

References 21 publications

Role of Metabolic Reprogramming in Epithelial–Mesenchymal Transition (EMT)

Role of Metabolic Reprogramming in Epithelial–Mesenchymal Transition (EMT)

Deregulation of Lipid Metabolism: The Critical Factors in Ovarian Cancer

Diosgenin inhibits the epithelial‑mesenchymal transition initiation in osteosarcoma cells via the p38MAPK signaling pathway

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