Induction of cyclooxygenase-2 expression by prostaglandin E2 stimulation of the prostanoid EP4 receptor via coupling to Gαi and transactivation of the epidermal growth factor receptor in HCA-7 human colon cancer cells

Yoshida, Kenji; Fujino, Hiromichi; Otake, Sho; Seira, Naofumi; Regan, John W.; Murayama, Toshihiko

doi:10.1016/j.ejphar.2013.08.002

Cited by 23 publications

(27 citation statements)

References 35 publications

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“…In contrast, COX-2 was not induced in HCA-7 cells by the EP2 or EP3 receptor agonists butaprost or sulprostone, respectively. 42) Of particular importance, the induction of COX-2 by PGE 2 -activated EP4 receptors in HCA-7 cells is primarily mediated by coupling of the receptor to G i -protein followed by the activation of PI3K and ERKs, which is consistent with the findings from the HEK cell model system as noted above.…”

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemsupporting

confidence: 79%

“…1B). Intriguingly, it has also been found that the EP4 receptor/G i -protein/PI3K-induced COX-2 pathway is not completely linear and another signaling pathway, a cAMP/ PKA line to CREB activation, 42) may also be involved, as previously reported (Fig. 1B).…”

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemsupporting

confidence: 49%

“…42) Moreover, the EP3/EP4 receptor agonist prostaglandin E 1 -alcohol induced COX-2 expression in HCA-7 cells. In contrast, COX-2 was not induced in HCA-7 cells by the EP2 or EP3 receptor agonists butaprost or sulprostone, respectively.…”

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemmentioning

confidence: 99%

“…The pathway was also shown to involve the transactivation of epidermal growth factor (EGF) receptors following the induction of metalloproteinase activity and the production of the EGF receptor ligand heparin-binding EGF-like growth factor 42) (Fig. 1B).…”

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemmentioning

confidence: 99%

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The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

Fujino

2016

Biological & Pharmaceutical Bulletin

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The lipid mediator prostanoids consist of prostaglandins and thromboxanes, and are synthesized from arachidonic acid by the action of cyclooxygenase. There are five major prostanoids, including prostaglandin E 2 (PGE 2 ), and they are involved in a variety of biological responses such as inflammation, allergy, parturition, and tumorigenesis. These prostanoids exert their effects via activation of their cognate G protein coupled receptors, e.g., E-type prostanoid (EP) receptors for PGE 2 . The EP receptors are composed of four subtypes, namely EP1 to EP4. Here, breakthroughs in the last dozen years of research are introduced, with a special focus on some important findings of EP4 receptor-mediated signaling and the signaling associated with cancer development, particularly in colon cancer.

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Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemsupporting

confidence: 79%

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemsupporting

confidence: 49%

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemmentioning

confidence: 99%

Section: Brief Sketch Of Findings Using Hca-7 Colon Cancer Cell Systemmentioning

confidence: 99%

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The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

Fujino

2016

Biological & Pharmaceutical Bulletin

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“…However, expression of EGFR in ESCC patients ranges between 4 and 86% [33–35]. Deregulation of EGFR plays an important role in tumor progression of lung [36], breast [37], gastrointestinal [38], and liver carcinoma [39]. Musashi1 is also expressed in different malignancies such as colorectal [40], endometrial [41], bladder [42], and esophageal cancers [43].…”

Section: Discussionmentioning

confidence: 99%

WNT and NOTCH signaling pathways as activators for epidermal growth factor receptor in esophageal squamous cell carcinoma

et al. 2018

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BackgroundEsophageal squamous cell carcinoma (ESCC) is the most common histological type of esophageal cancer, with a poor prognosis. Deregulation of WNT and NOTCH signaling pathways is important in ESCC progression, which can be due to either malfunction of their components or crosstalk with other pathways. Therefore, identification of new crosstalk between such pathways may be effective to introduce new strategies for targeted therapy of cancer. A correlation study was performed to assess the probable interaction between growth factor receptors and WNT/NOTCH pathways via the epidermal growth factor receptor (EGFR) and Musashi1 (MSI1), respectively.MethodsLevels of MSI1/EGFR mRNA expression in tumor tissues from 48 ESCC patients were compared to their corresponding normal tissues using real-time polymerase chain reaction.ResultsThere was a significant correlation between EGFR and MSI1 expression (p = 0.05). Moreover, there was a significant correlation between EGFR/MSI1 expression and grade of tumor differentiation (p = 0.02).ConclusionThis study confirms a direct correlation between MSI1 and EGFR and may support the important role of MSI1 in activation of EGFR through NOTCH/WNT pathways in ESCC.

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PGE₁ and E₃ show lower efficacies than E₂ to β‐catenin‐mediated activity as biased ligands of EP4 prostanoid receptors

et al. 2017

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The 2-series of prostaglandin E (PGE ) is regarded as a pro-cancer prostanoid, whereas the 1-series (PGE ) and the 3-series (PGE ) are considered to act as anti-cancer prostanoids. In the present study, we provide possible reasons why PGE and PGE , but not PGE , exert anti-cancer effects by focusing on each diverged E-type prostanoid (EP)4 receptor-mediated signaling pathway. PGE , PGE and PGE function as full agonists in terms of G - and G -protein-mediated signaling. However, PGE and PGE function as partial agonists of T-cell factor (TCF)/β-catenin (β-cat)-mediated activity, the well-known cancer-related signaling pathway. Furthermore, pretreatment with PGE or PGE almost completely reduces PGE -induced TCF/β-cat activity. These results provide a plausible reason why PGE and PGE function as anti-cancer prostanoids as a result of novel biased activity for EP4 receptors.

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Induction of cyclooxygenase-2 expression by prostaglandin E2 stimulation of the prostanoid EP4 receptor via coupling to Gαi and transactivation of the epidermal growth factor receptor in HCA-7 human colon cancer cells

Cited by 23 publications

References 35 publications

The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

WNT and NOTCH signaling pathways as activators for epidermal growth factor receptor in esophageal squamous cell carcinoma

PGE₁ and E₃ show lower efficacies than E₂ to β‐catenin‐mediated activity as biased ligands of EP4 prostanoid receptors

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Induction of cyclooxygenase-2 expression by prostaglandin E2 stimulation of the prostanoid EP4 receptor via coupling to Gαi and transactivation of the epidermal growth factor receptor in HCA-7 human colon cancer cells

Cited by 23 publications

References 35 publications

The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

The Roles of EP4 Prostanoid Receptors in Cancer Malignancy Signaling

WNT and NOTCH signaling pathways as activators for epidermal growth factor receptor in esophageal squamous cell carcinoma

PGE1 and E3 show lower efficacies than E2 to β‐catenin‐mediated activity as biased ligands of EP4 prostanoid receptors

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PGE₁ and E₃ show lower efficacies than E₂ to β‐catenin‐mediated activity as biased ligands of EP4 prostanoid receptors