Y‐box binding protein‐1 is a novel molecular target for tumor vessels

Takahashi, Mamoru; Shimajiri, Shohei; Izumi, Hiroto; Hirano, Gen; Kashiwagi, Eiji; Yasuniwa, Yoshihiro; Wu, Ying; Han, Bo; Akiyama, Masaki; Nishizawa, Shigeru; Sasaguri, Yasuyuki; Kohno, Kimitoshi

doi:10.1111/j.1349-7006.2010.01534.x

Cited by 41 publications

(25 citation statements)

References 32 publications

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“…In addition, several genes important for wound healing and cellular proliferation and survival are regulated by YB-1, including collagen alpha1 and alpha2 (Norman et al 2001;Higashi et al 2003), matrix metalloproteinase 2 (Mertens et al 1997), the B-chain isoform of plateletderived growth factor (Stenina et al 2000), vascular endothelial growth factor (Coles et al 2004), granulocyte-macrophage-colony stimulating factor (Coles et al 2000), and Fas death receptor (Lasham et al 2000); moreover, YB-1 can also regulate αSMA and human pulmonary myofibroblasts (Zhang et al 2005). Takahashi et al (2010) reported that YB-1 is increased in the angiogenic endothelial cells of various tumors and is involved in the growth of endothelial cells. These previous findings suggest the possibility that YB-1 is involved in tissue regeneration in various situations in vivo, including tissue regeneration after ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Y-Box-Binding Protein-1 in Hind-Limb Muscles During Regeneration from Ischemic Injury in Mice

Fuke

Narita

Wada

et al. 2018

Tohoku J. Exp. Med.

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Critical limb ischemia (CLI) is the most severe complication of peripheral arterial disease (PAD). Understanding the molecular mechanisms underlying tissue repair after CLI is necessary for preventing PAD progression. Y-box binding protein-1 (YB-1) regulates the expression of many genes in response to environmental stresses. We aimed to determine whether YB-1 is involved in ischemic muscle regeneration. A mouse ischemic hind-limb model was generated; namely, the femoral, saphenous, and popliteal arteries in the left hind limb were ligated. The right hind limb, with skin incisions alone, served as control. Hind limbs (n = 3-5 for each time point) were examined on day 0 (before the operation) and on postoperative days 1, 2, 7, 10, and 14, and the biceps femoris, adductor, rectus femoris, and gracilis muscles were subjected to histopathological and immunohistochemical analyses. In ischemic limbs, myogenesis, triggered by an increase in myotubes, began on day 7; thereafter, regenerated muscles gradually increased in volume. RT-PCR analysis showed that YB-1 mRNA levels were increased in the limbs after ischemic injury, peaked on day 2, and subsequently decreased. On day 7, expression levels of MyoD and alphasmooth muscle actin (αSMA) mRNAs were significantly higher in ischemic muscles than in control muscles. Immunohistochemical analysis revealed increased YB-1 immunoreactivity in myoblasts and myotubes on day 7, which was decreased by day 14. The immunoreactive αSMA and smooth muscle myosin heavy chain were transiently increased in myotubes. This is the first report showing the increased expression of YB-1 during muscle regeneration after ischemic injury.

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Y-Box-Binding Protein-1 in Hind-Limb Muscles During Regeneration from Ischemic Injury in Mice

Fuke

Narita

Wada

et al. 2018

Tohoku J. Exp. Med.

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“…1), it seems very likely that overexpression of hPRDX4 in the atherosclerotic aorta protects against chronic inflammation and subsequent disease progression by preventing inflammatory cell-derived ROS generation and scavenging the generated extracellular pool of ROS. Indeed, we detected lower levels of 8-OHdG, oxLDL, and circulating TBARS as markers of oxidative stress (3,21,23) (Fig. 4), and reduced cellularity of macrophages as secretory cells in the fibrous caps of the atheromas (Supplementary Table S1) in HcD-fed hPRDX4…”

Section: Role Of Prdx4 In Atherosclerosismentioning

confidence: 99%

“…For the monoclonal mouse a-SMA antibody, we treated sections with the HistoMouse TM -Plus Kit (Invitrogen Corporation, Camarillo, CA) to block endogenous IgG. Double IHC was also performed to detect the distribution of both hPRDX4-and a-SMA-positive SMCs or both hPRDX4-and Mac-2-positive macrophages in atherosclerotic lesions (hPRDX4 with Vulcan Fast Red and a-SMA or Mac-2 with DAB as a substrate, respectively) using the MACH 2 Double Stain system (Biocare Medical) (3,23).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Overexpression of Peroxiredoxin 4 Attenuates Atherosclerosis in Apolipoprotein E Knockout Mice

Guo

Yamada²,

Tanimoto³

et al. 2012

Antioxidants & Redox Signaling

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141

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Aim: A growing body of evidence has shown that increased formation of oxidized molecules and reactive oxygen species within the vasculature (i.e., the extracellular space) plays a crucial role in the initiation and progression of atherosclerosis and in the formation of unstable plaques. Peroxiredoxin 4 (PRDX4) is the only known secretory member of the antioxidant PRDX family. However, the relationship between PRDX4 and susceptibility to atherosclerosis has remained unclear. Results: To define the role of PRDX4 in hyperlipidemia-induced atherosclerosis, we generated hPRDX4 transgenic (Tg) and apolipoprotein E (apoE) knockout mice (hPRDX4 +/+ /apoE -/ -). After feeding the mice a high-cholesterol diet, they showed fewer atheromatous plaques, less T-lymphocyte infiltration, lower levels of oxidative stress markers, less necrosis, a larger number of smooth muscle cells, and a larger amount of collagen, resulting in thickened fibrous cap formation and possible stable plaque phenotype as compared with apoE -/ -mice. We also detected greater suppression of apoptosis and decreased Bax expression in hPRDX4 +/+ /apoE -/ -mice than in apoE -/ -mice. Bone marrow transplantation from hPRDX4 +/+ donors to apoE -/ -mice confirmed the antiatherogenic aspects of PRDX4, revealing significantly suppressed atherosclerotic progression. Innovation: In this study, we demonstrated for the first time that PRDX4 suppressed the development of atherosclerosis in apoE -/ -mice fed a high-cholesterol diet. Conclusion: These data indicate that PRDX4 is an antiatherogenic factor and, by suppressing oxidative damage and apoptosis, that it may protect against the formation of vulnerable (unstable) plaques. Antioxid. Redox Signal. 17, 1362-1375.

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“…The cell proliferation assay has been previously described. (17) Briefly, siRNA-transfected A110L cells were seeded into 12-well plates at a density of 1 · 10 4 cells per well. Twenty-four hours after transfection was set as time zero.…”

Section: Methodsmentioning

confidence: 99%

Monocarboxylate transporters 1 and 4 are involved in the invasion activity of human lung cancer cells

Izumi

Takahashi²,

Uramoto³

et al. 2011

Cancer Science

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153

136

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Cancer cells show constitutive upregulation of glycolysis, and the concentration of lactate thus produced correlates with prognosis. Here, we examined whether lactate concentration and lactate transporter expression are related to migration and invasion activity. We found that the expression of the monocarboxylate transporters MCT1 and MCT4, but not MCT5, in human lung cancer cell lines was significantly correlated with invasiveness. To clarify the effects of MCT1 and MCT4 expression on invasion, we performed migration and invasion assays after transfection with siRNA specific for MCT1 or MCT4. Knockdown of MCT1 or MCT4 did not influence cell migration but reduced invasion; this was also observed for knockdown of the lactate transporter-associated protein basigin. We also demonstrated that both expression and activity of MMP9 and MMP2 were not correlated with invasion activity and not regulated by MCT1, MCT4 and basigin. Furthermore, the addition of lactate did not increase migration and invasion activity, but low concentration of 4,4¢-diisothiocyanatostilbene-2,2¢-disulphonic acid (DIDS), a general anion channel blocker, as well as other MCT inhibitors quercetin and simvastatin, inhibited cell invasion without influencing migration activity and the cellular expression of MCT1 and MCT4. This is the first report suggesting that lactate transporters are involved in human cancer cell invasiveness. As such, these proteins may be promising targets for the prevention of cancer invasion and metastasis. (Cancer Sci 2011; 102: 1007-1013 M onocarboxylates, such as lactate and pyruvate, play a central role in cellular metabolism and metabolic communication between tissues.(1) In cancer cells, a steady source of metabolic energy is required to continue the uncontrolled growth and proliferation of these cells.(2) Most cancer cells rely on a high rate of aerobic glycolysis, a phenomenon termed ''the Warburg effect'', to obtain sufficient ATP in a hypoxic microenvironment.(3) As a result of the Warburg effect, lactate is abundantly synthesized from pyruvate, (4) but lactic acid induces cellular acidosis, which triggers apoptosis. To avoid apoptosis, cancer cells must transport the lactate out of the cell. On the other hand, lactate is not just a waste product: it was recently identified as a major energy fuel in tumors.(4) Lactate is transported by monocarboxylate anion transporters (MCT; also called the solute carrier family 16 [SLC16]).(1) It is known that MCT4 (SLC16A3) transports lactate out of the cell (5) and MCT1 (SLC16A1) regulates the entry of lactate into tumor cells. (4) Migration and invasion are two of the most important aspects of the malignant cancer phenotype; if they could be inhibited, the cancer prognosis would improve. Hypoxia and acidosis create a nurturing environment for tumor progression and the evolution of metastases, and invasiveness is abetted by acidosis, the result of shifting to an anaerobic glycolytic metabolism.(6) Basigin (BSG; also called EMMPRIN and CD147) is a multifunctional glycoprotein ...

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Y‐box binding protein‐1 is a novel molecular target for tumor vessels

Cited by 41 publications

References 32 publications

Increased Expression of Y-Box-Binding Protein-1 in Hind-Limb Muscles During Regeneration from Ischemic Injury in Mice

Increased Expression of Y-Box-Binding Protein-1 in Hind-Limb Muscles During Regeneration from Ischemic Injury in Mice

Overexpression of Peroxiredoxin 4 Attenuates Atherosclerosis in Apolipoprotein E Knockout Mice

Monocarboxylate transporters 1 and 4 are involved in the invasion activity of human lung cancer cells

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