Prostaglandin E<sub>2</sub> reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP<sub>3</sub>

Yano, Tomohiro; Zissel, Gernot; Muller-Qernheim, Joachim; Shin, Sung Jae; Satoh, Haruna; Ichikawa, Tomio

doi:10.1016/s0014-5793(02)02689-3

Cited by 60 publications

(43 citation statements)

References 18 publications

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“…33 The MAPK pathway, on the other hand, seems to induce COX-2 production generating a positive feedback cycle. 34 The same pathway may even activate the production of epithelial growth factor (EGF) in colorectal tumors. 35 Another property of COX-2 related to carcinogenesis is the promotion of tumor angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Oral acetylsalicylic acid and prevalence of actinic keratosis

Schmitt

Miot

2014

Rev. Assoc. Med. Bras.

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Section: Discussionmentioning

confidence: 99%

Oral acetylsalicylic acid and prevalence of actinic keratosis

Schmitt

Miot

2014

Rev. Assoc. Med. Bras.

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“…Total RNA was isolated using a ChargeSwitch ® Total RNA Cell kit (Invitrogen), and cDNA was synthesized as previously described (21 Assessment of anchorage-dependent and anchorageindependent cell growth Anchorage-dependent growth rate was measured by determining the cell count. Cells were seeded in a 96-well plate (5.0 × 10 4 cells /well) and cultured.…”

Section: Isolation Of Total Rna and Real-time Rt-pcrmentioning

confidence: 99%

Enhanced Effect of Connexin 43 on Cisplatin-Induced Cytotoxicity in Mesothelioma Cells

et al. 2009

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Abstract. The expression levels of connexin (Cx) proteins, which are gap junction (GJ) components, are often decreased in many cancers, and restoring their levels has been shown to have antitumor effects. Previously, dysfunctional gap junctional intercellular communication (GJIC) has been observed in several malignant mesotheliomas (MMs), and among the many Cx proteins, Cx43 is prominently expressed in nontumorigenic mesothelial tissues. Therefore, we investigated whether Cx43 upregulation has an antitumor effect on an MM cell line (H28 cell), especially with regard to drug resistance. After treatment with the chemotherapeutic agent cisplatin (CDDP), MM cell viability significantly decreased, and apoptosis induction was observed in Cx43-transfected clones. A specific GJIC inhibitor could not abrogate this effect. On the other hand, the Src protein is known to phosphorylate Cx43, which results in GJIC inhibition. This suggests that Src activity might also be regulated by the hyperexpression of Cx43. In fact, the Src protein level was decreased in Cx43-transfected clones. Moreover, Src inhibition reinforced CDDP cytotoxicity in parental H28 cells. These data suggest that Cx43 could improve the resistance to CDDP in a GJIC-independent manner, which may be partly mediated by the suppression of Src activity.

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“…Total RNA was isolated from cultured A549 cells as described previously [17] [174][175][176][177][178][179][180][181][182][183][184][185][186][187][188][189][190][191][192][193], antisense primer (nucleotides 313-332). GAPDH was used as an internal control.…”

Section: Rt-pcrmentioning

confidence: 99%

Peroxisome proliferator‐activated receptor δ as a molecular target to regulate lung cancer cell growth

et al. 2005

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It has been assumed that prostaglandin (PG)I 2 signaling contributes to the negative growth control of lung cancer cells; however, the mechanism remains unresolved. PGI 2 functions through a cell surface G protein-coupled receptor (prostaglandin I2-binding receptor, IP) and also exerts an effect by interacting with a nuclear hormone receptor, peroxisome proliferator-activated receptor d (PPARd). We found that PPARd was a key molecule of PGI 2 signaling to give negative growth control of lung cancer cells (A549), using carbarprostacyclin, a PGI 2 agonist for IP and PPARd, and L-165041, a PPARd agonist. Furthermore, PPARd-induced cell growth control was reinforced by the inhibition of cyclooxygenase. These results suggest that PPARd activation under the suppression of PG synthesis is important to regulate lung cancer cell growth.

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Prostaglandin E₂ reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP₃

Cited by 60 publications

References 18 publications

Oral acetylsalicylic acid and prevalence of actinic keratosis

Oral acetylsalicylic acid and prevalence of actinic keratosis

Enhanced Effect of Connexin 43 on Cisplatin-Induced Cytotoxicity in Mesothelioma Cells

Peroxisome proliferator‐activated receptor δ as a molecular target to regulate lung cancer cell growth

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Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3

Cited by 60 publications

References 18 publications

Oral acetylsalicylic acid and prevalence of actinic keratosis

Oral acetylsalicylic acid and prevalence of actinic keratosis

Enhanced Effect of Connexin 43 on Cisplatin-Induced Cytotoxicity in Mesothelioma Cells

Peroxisome proliferator‐activated receptor δ as a molecular target to regulate lung cancer cell growth

Contact Info

Product

Resources

About

Prostaglandin E₂ reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP₃