Lysophosphatidylethanolamine stimulates chemotactic migration and cellular invasion in SK‐OV3 human ovarian cancer cells: Involvement of pertussis toxin‐sensitive G‐protein coupled receptor

Park, Kyoung Sun; Lee, Ha Young; Lee, Sun Young; Kim, Mi-Kyoung; Kim, Sang Doo; Kim, Jung Mo; Yun, Jeanho; Im, Dong‐Soon; Bae, Yoe‐Sik

doi:10.1016/j.febslet.2007.08.014

Cited by 92 publications

(81 citation statements)

References 23 publications

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“…While higher expression of LPA-1 was reported in OVCAR-3 cells, LPA3 is the major receptor type in SKOV-3 cells (Park et al, 2007). In the present study, we showed that LPA2 expression is higher than other types of LPA receptor in CAOV-3 cells.…”

Section: Discussionsupporting

confidence: 55%

Lysophosphatidic acid receptor 2 and Gi/Src pathway mediate cell motility through cyclooxygenase 2 expression in CAOV-3 ovarian cancer cells

et al. 2008

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Lysophosphatidic acid (LPA) is a bioactive phospholipids and involves in various cellular events, including tumor cell migration. In the present study, we investigated LPA receptor and its transactivation to EGFR for cyclooxygenase-2 (COX-2) expression and cell migration in CAOV-3 ovarian cancer cells. LPA induced COX-2 expression in a dose-dependent manner, and pretreatment of the cells with pharmacological inhibitors of Gi (pertussis toxin), Src (PP2), EGF receptor (EGFR) (AG1478), ERK (PD98059) significantly inhibited LPA-induced COX-2 expression. Consistent to these results, transfection of the cells with selective Src siRNA attenuated COX-2 expression by LPA. LPA stimulated CAOV-3 cell migration that was abrogated by pharmacological inhibitors and antibody of EP2.Higher expression of LPA2 mRNA was observed in CAOV-3 cells, and transfection of the cells with a selective LPA2 siRNA significantly inhibited LPA-induced activation of EGFR and ERK, as well as COX-2 expression. Importantly, LPA2 siRNA also blocked LPA-induced ovarian cancer cell migration. Collectively, our results clearly show the significance of LPA2 and Gi/Src pathway for LPA-induced COX-2 expression and cell migration that could be a promising drug target for ovarian cancer cell metastasis.

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Section: Discussionsupporting

confidence: 55%

Lysophosphatidic acid receptor 2 and Gi/Src pathway mediate cell motility through cyclooxygenase 2 expression in CAOV-3 ovarian cancer cells

et al. 2008

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“…Although only a few papers have reported the physiological function of LPE to date, LPE might modulate several biological responses, possibly through G-protein-coupled receptor. 34 On the other hand, LPI is thought to be produced from phosphatidylinositol in activated platelets, 27 and its involvement in the migration of smooth muscle cells has been proposed. 35 Recently, a series of elegant studies have demonstrated that the state of cell activation and the autotaxin levels may determine the production of LPA.…”

Section: Discussionmentioning

confidence: 99%

Possible Involvement of Minor Lysophospholipids in the Increase in Plasma Lysophosphatidic Acid in Acute Coronary Syndrome

Kurano

Suzuki

Inoue

et al. 2015

ATVB

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Objective-Lysophosphatidic acids (LPA) have important roles in the field of vascular biology and are derived mainly from lysophosphatidylcholine via autotaxin. However, in our previous study, only the plasma LPA levels, and not the serum autotaxin levels, increased in patients with acute coronary syndrome (ACS). The aim of this study was to elucidate the pathway by which LPA is increased in patients with ACS. Approach and Results-We measured the plasma lysophospholipids species in 141 consecutive patients undergoing coronary angiography (ACS, n=38; stable angina pectoris, n=71; angiographically normal coronary arteries, n=32) using a liquid chromatography-tandem mass spectrometry analysis. Among the ACS subjects, notable increases in the 22:6 LPA, 18:2 LPA, and 20:4 LPA levels were observed. The in vitro experiments revealed that serum incubation mainly increased the 18:2 LPA level, whereas platelet activation increased the 20:4 LPA level. Minor lysophospholipids other than LPA were also elevated in ACS subjects and were well correlated with the corresponding LPA species, including 22:6 LPA. A multiple regression analysis also revealed that lysophosphatidylinositol, lysophosphatidylcholine, lysophosphatidylethanolamine, and lysophosphatidylglycerol were independent explanatory variables for several LPA species. Conclusions-Specific LPA species, especially long-chain unsaturated LPA, were elevated in ACS patients, along with the corresponding minor lysophospholipids. The elevation of these LPA species might be mainly caused by presently unidentified LPA-producing pathway(s). Minor lysophospholipids might be involved in the generation of LPA, especially 22:6 LPA, and in the pathogenesis of ACS. LPA levels were elevated in patients with ACS but not in those with stable angina pectoris (SAP). 16 This result suggested that LPA might be involved in plaque instability and platelet activation in human subjects. In addition, we also found that serum autotaxin levels were not elevated in patients with ACS; LPA is hydrolyzed from lysophosphatidylcholine (LPC) by autotaxin/lysophospholipase D. 17 This discrepancy between LPA and autotaxin interested us greatly because autotaxin is a key enzyme in the production of LPA. Actually, we previously reported a strong positive correlation between LPA and autotaxin in healthy subjects, 18 patients with chronic hepatitis, 19 and patients with follicular lymphoma.20 Therefore, the discordance between ACS subjects and other subjects prompted us to investigate the origins of the elevation in LPA in patients with ACS.LPA is structurally composed of a fatty acid linked to snglycerol-3 phosphate, and the molecular species of the fatty acid chain are varied and determine the molecular species of LPA. In a previous report, 16 we measured the total LPA and LPC levels using previously described enzymatic methods. 21 Using these methods, we could not obtain any information concerning which molecular species of LPA were elevated in patients with ACS. To overcome this limitation, we determined th...

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“…Recent studies have shown that mRNA of TRPV2 is expressed in prostate (18). TRPV2 function may be regulated by some lysophospholipids identified and known to have a range of physiologic and pathologic effects, including stimulation of cancer cell migration (19)(20)(21). However, the question remains as to how TRPV2 is involved in tumor development and progression both in vitro and in vivo to an extremely aggressive castration-resistant stage and whether it could be a real hallmark of poor prognosis in patients suffering from PCa.…”

Section: Introductionmentioning

confidence: 99%

Role of Cationic Channel TRPV2 in Promoting Prostate Cancer Migration and Progression to Androgen Resistance

et al. 2010

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Castration resistance in prostate cancer (PCa) constitutes an advanced, aggressive disease with poor prognosis, associated with uncontrolled cell proliferation, resistance to apoptosis, and enhanced invasive potential. The molecular mechanisms involved in the transition of PCa to castration resistance are obscure. Here, we report that the nonselective cationic channel transient receptor potential vanilloid 2 (TRPV2) is a distinctive feature of castration-resistant PCa. TRPV2 transcript levels were higher in patients with metastatic cancer (stage M1) compared with primary solid tumors (stages T2a and T2b). Previous studies of the TRPV2 channel indicated that it is primarily involved in cancer cell migration and not in cell growth. Introducing TRPV2 into androgen-dependent LNCaP cells enhanced cell migration along with expression of invasion markers matrix metalloproteinase (MMP) 9 and cathepsin B. Consistent with the likelihood that TRPV2 may affect cancer cell aggressiveness by influencing basal intracellular calcium levels, small interfering RNA-mediated silencing of TRPV2 reduced the growth and invasive properties of PC3 prostate tumors established in nude mice xenografts, and diminished expression of invasive enzymes MMP2, MMP9, and cathepsin B. Our findings establish a role for TRPV2 in PCa progression to the aggressive castration-resistant stage, prompting evaluation of TRPV2 as a potential prognostic marker and therapeutic target in the setting of advanced PCa. Cancer Res; 70(3); 1225-35. ©2010 AACR.

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Lysophosphatidylethanolamine stimulates chemotactic migration and cellular invasion in SK‐OV3 human ovarian cancer cells: Involvement of pertussis toxin‐sensitive G‐protein coupled receptor

Cited by 92 publications

References 23 publications

Lysophosphatidic acid receptor 2 and Gi/Src pathway mediate cell motility through cyclooxygenase 2 expression in CAOV-3 ovarian cancer cells

Lysophosphatidic acid receptor 2 and Gi/Src pathway mediate cell motility through cyclooxygenase 2 expression in CAOV-3 ovarian cancer cells

Possible Involvement of Minor Lysophospholipids in the Increase in Plasma Lysophosphatidic Acid in Acute Coronary Syndrome

Role of Cationic Channel TRPV2 in Promoting Prostate Cancer Migration and Progression to Androgen Resistance

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