Linoleic Acid Attenuates Endothelium-Derived Relaxing Factor Production by Suppressing cAMP-Hydrolyzing Phosphodiesterase Activity

Wei, Jiazhang; Takeuchi, Kazuhiko; Watanabe, Hiroshi

doi:10.1253/circj.cj-13-0248

Cited by 8 publications

(6 citation statements)

References 34 publications

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“…Cytosolic Ca 2+ concentration ([Ca 2+ ] cyt ) was measured in individual serum-deprived cells over a time course using a membrane-permeable fluorescent Ca 2+ indicator, namely, the acetoxymethyl ester of fura-2 (fura-2-AM) (Dojindo Molecular Technologies, Inc, Kumamoto, Japan), as described in our previous studies. 7 – 9 , 12 …”

Section: Methodsmentioning

confidence: 99%

Blockage of store-operated Ca2+ entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca2+ signaling-regulated VEGF production in nasopharyngeal carcinoma

Ye¹,

Huang²,

He³

et al. 2018

CMAR

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BackgroundEpstein–Barr virus (EBV) actively contributes to the pathological process of nasopharyngeal carcinoma (NPC) by enabling NPC cells to acquire various capacities required for their malignant biological actions. Our earlier works demonstrated that EBV-encoded latent membrane protein 1 (LMP1) enhanced vascular endothelial growth factor (VEGF)-mediated angiogenesis by boosting store-operated Ca2+ entry (SOCE) upon extracellular epidermal growth factor (EGF) stimulation. However, the antagonistic effects of SOCE blockage on EBV-promoted angiogenesis must be appropriately evaluated in vivo, and the global effect of EBV infection on the EGF-elicited cytosolic Ca2+ signaling, which regulates VEGF-mediated angiogenesis remains to be further clarified.Materials and methodsTwo EBV-infected NPC cell lines, CNE2-EBV and HK1-EBV, along with their parental cell lines were employed in the present study. Dynamic cytosolic Ca2+ changes were measured in individual fluorescent Ca2+ indicator-loaded cells. Amounts of VEGF production were determined by enzyme-linked immunosorbent assay (ELISA). Human umbilical vein endothelial cells (HUVECs)-formed tube networks were quantitatively evaluated as an in vitro angiogenesis assay. A mouse model concurrently bearing EBV-positive/negative xenografts was utilized to evaluate the tumor growth and angiogenesis in vivo.ResultsEBV infection reliably promoted transplanted tumor growth while enhancing angiogenesis. Introduction of EBV into EBV-negative NPC cells increased the EGF-stimulated VEGF production while amplifying the EGF-evoked Ca2+ responses. Inhibition of the EBV-boosted Ca2+ signaling using 2-aminoethyl diphenylborinate (2-APB), a specific SOCE inhibitor, effectively antagonized the EBV-promoted VEGF production and endothelial tube formation in vitro. Pharmacological blockage of SOCE exhibited anti-angiogenic effect in the EBV-positive xenografts.ConclusionSOCE can serve as a candidate pharmacological target for treating NPC, as blockage of the Ca2+ signaling via SOCE is a feasible strategy to suppress the EBV-driven malignant profiles in NPC cells.

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Section: Methodsmentioning

confidence: 99%

Blockage of store-operated Ca2+ entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca2+ signaling-regulated VEGF production in nasopharyngeal carcinoma

Ye¹,

Huang²,

He³

et al. 2018

CMAR

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“…[Ca 2+ ] cyto was measured in individual NPC cells utilizing a fluorescent Ca 2+ indicator, the acetoxymethyl ester of fura-2 (fura-2/AM; Dojindo Molecular Technologies, Inc., Kumamoto, Japan), as described in our previous studies. 11 , 14 , 15 The absorption shift of fura-2 that occurs upon binding can be determined by scanning the excitation spectrum between 340 nm and 380 nm while monitoring the emission at 510 nm. Fluorescent images were acquired and quantified from the individual fura-2-loaded cells with a fluorescence imaging and analysis system (Aqua Cosmos 2.6; Hamamatsu Photonics, Hamamatsu, Japan).…”

Section: Methodsmentioning

confidence: 99%

SKF95365 induces apoptosis and cell-cycle arrest by disturbing oncogenic Ca2+ signaling in nasopharyngeal carcinoma cells

Zhang

Wei

et al. 2015

OTT

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. SKF96365 promoted cell mortality, inhibited colony formation, and induced apoptosis and cell-cycle arrest, while blunting the EGF-evoked Ca 2+ signaling. Furthermore, we confirmed that SKF96365 reduced NPC xenograft growth while activating caspase-7-related apoptotic pathway. Conclusion: SKF96365 exerts multiple antitumor activities through the distraction on the oncogenic Ca 2+ signaling transduction in NPC cells.

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“…Cytosolic Ca 2+ concentration ([Ca 2+ ]cyto) was measured in individual NPC cells by using an fluorescent Ca 2+ indicator, acetoxymethyl ester of fura-2 (fura-2/AM) (Dojindo Molecular Technologies, Inc., Kumamoto, Japan), as our previous description [13,22,23].…”

Section: Measurement Of Cytosolic Ca 2+ Concentration ([Ca 2+ ]Cyto)mentioning

confidence: 99%

Blockage of LMP1-modulated store-operated Ca2+ entry reduces metastatic potential in nasopharyngeal carcinoma cell

Wei

Zhang

et al. 2015

Cancer Letters

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Linoleic Acid Attenuates Endothelium-Derived Relaxing Factor Production by Suppressing cAMP-Hydrolyzing Phosphodiesterase Activity

Cited by 8 publications

References 34 publications

Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma

Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma

SKF95365 induces apoptosis and cell-cycle arrest by disturbing oncogenic Ca2+ signaling in nasopharyngeal carcinoma cells

Blockage of LMP1-modulated store-operated Ca2+ entry reduces metastatic potential in nasopharyngeal carcinoma cell

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Linoleic Acid Attenuates Endothelium-Derived Relaxing Factor Production by Suppressing cAMP-Hydrolyzing Phosphodiesterase Activity

Cited by 8 publications

References 34 publications

Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein&ndash;Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma

Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein&ndash;Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma

SKF95365 induces apoptosis and cell-cycle arrest by disturbing oncogenic Ca2+ signaling in nasopharyngeal carcinoma cells

Blockage of LMP1-modulated store-operated Ca2+ entry reduces metastatic potential in nasopharyngeal carcinoma cell

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Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma

Blockage of store-operated Ca<sup>2+</sup> entry antagonizes Epstein–Barr virus-promoted angiogenesis by inhibiting Ca<sup>2+</sup> signaling-regulated VEGF production in nasopharyngeal carcinoma