Expression of Stress-Response and Cell Proliferation Genes in Renal Cell Carcinoma Induced by Oxidative Stress

Tanaka, Tomoyuki; Kondo, Shohei; Iwasa, Yoko; Hayashi, Hiroshi; Toyokuni, Shinya

doi:10.1016/s0002-9440(10)65085-7

Cited by 61 publications

(35 citation statements)

References 52 publications

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“…The anchor primer was 5 0 -CCCGGATCCd(T) 15 V-3 0 labeled with rhodamine at its 5 0 end. FDD was carried out as previously described (Tanaka et al, 2000). A measure of 5 ml aliquots of each polymerase chain reaction (PCR) product were analysed by electrophoresis on 4% polyacrylamide gels in 7 M urea at 40 W constant power for 2-3 h. DNA in the gels was visualized using FMBIO-100 (Takara Bio, Shiga).…”

Section: Rna Isolation and Fdd Analysismentioning

confidence: 99%

“…However, since no occurrence of RCC has been observed in p16 knockout mice studies (Serrano et al, 1996;Krimpenfort et al, 2001;Sharpless et al, 2001), other alterations might also play a role in oxidative stress-induced carcinogenesis. In a more recent attempt to find the gene(s) responsible for Fe-NTAinduced RCCs, we modified a fluorescent differential display (FDD) technique, and by screening approximately 84 000 transcripts isolated 20 differentially expressed clones, including annexin 2 (Anx2; p36, lipocortin II, chromobindin VIII or placental anticoagulant protein IV) (Tanaka et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis

et al. 2004

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Section: Rna Isolation and Fdd Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis

et al. 2004

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“…Expression has also been reported in proximal tubule cells, but primarily only in response to insults, mitogens, or second messengers (14,20,41,45,62,63). There is a dearth of information regarding IGFBP7 in the kidney, and what is available is contradictory, showing expression in the glomerulus and alternatively in distal and proximal tubule cells (17,35,42,65,72).…”

mentioning

confidence: 99%

Insulin-like growth factor binding protein 7 and tissue inhibitor of metalloproteinases-2: differential expression and secretion in human kidney tubule cells

Emlet

Pastor-Soler

Marciszyn

et al. 2017

American Journal of Physiology-Renal Physiology

106

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We have characterized the expression and secretion of the acute kidney injury (AKI) biomarkers insulin-like growth factor binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2) in human kidney epithelial cells in primary cell culture and tissue. We established cell culture model systems of primary kidney cells of proximal and distal tubule origin and observed that both proteins are indeed expressed and secreted in both tubule cell types in vitro. However, TIMP-2 is both expressed and secreted preferentially by cells of distal tubule origin, while IGFBP7 is equally expressed across tubule cell types yet preferentially secreted by cells of proximal tubule origin. In human kidney tissue, strong staining of IGFBP7 was seen in the luminal brush-border region of a subset of proximal tubule cells, and TIMP-2 stained intracellularly in distal tubules. Additionally, while some tubular colocalization of both biomarkers was identified with the injury markers kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin, both biomarkers could also be seen alone, suggesting the possibility for differential mechanistic and/or temporal profiles of regulation of these early AKI biomarkers from known markers of injury. Last, an in vitro model of ischemia-reperfusion demonstrated enhancement of secretion of both markers early after reperfusion. This work provides a rationale for further investigation of these markers for their potential role in the pathogenesis of acute kidney injury.

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“…47 Furthermore, ANXA2 is known to be present in various cells such as endothelial cells, monocytes, macrophages, and most cancer cells. 39,48,49 Asbestos is neither an intracellular pathogen that has developed specific ligand proteins to enter nonprofessional phagocytes nor an apoptotic body that arises during the normal physiological state and has a phagocytic removal system through nonprofessional phagocytes. In addition, no counterpart to asbestos exists in vivo; therefore, it is unlikely that mesothelial cells have specific receptors that mediate asbestos phagocytosis without an opsonin effect, such as coating by vitronectin.…”

Section: Discussionmentioning

confidence: 99%

Receptor role of the annexin A2 in the mesothelial endocytosis of crocidolite fibers

Yamashita

Nagai

Toyokuni

2015

Laboratory Investigation

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Asbestos-induced mesothelioma is a worldwide problem. Parietal mesothelial cells internalize asbestos fibers that traverse the entire lung parenchyma, an action that is linked to mesothelial carcinogenesis. Thus far, vitronectin purified from serum reportedly enhances the internalization of crocidolite by mesothelial cells via integrin avb5. To reveal another mechanism by which mesothelial cells endocytose (phagocytose) asbestos, we first evaluated the effects of serum on asbestos uptake, which proved to be nonessential. Thereafter, we undertook a study to identify proteins on the surface of mesothelial cells (MeT5A) that act as receptors for asbestos uptake based on the assumption that receptors bind to asbestos with physical affinity. To this end, we incubated the membrane fraction of MeT5A cells with crocidolite or chrysotile and evaluated the adsorbed proteins using sodium dodecyl sulfate polyacrylamide gel analysis. Next, we extensively identified the proteins using an in-solution or in-gel digestion coupled with mass spectrometry. Among the identified proteins, annexin A2 (ANXA2) and transferrin receptor protein 1 (TFRC) were distinguished because of their high score and presence at the cell surface. Crocidolite uptake by MeT5A cells was significantly decreased by shRNA (short hairpin RNA)-induced knockdown of ANXA2 and direct blockade of cell surface ANXA2 using anti-ANXA2 antibody. In addition, abundant ANXA2 protein was present on the cell membrane of mesothelial cells, particularly facing the somatic cavity. These findings demonstrate that ANXA2 has a role in the mesothelial phagocytosis of crocidolite and may serve as its receptor.

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Expression of Stress-Response and Cell Proliferation Genes in Renal Cell Carcinoma Induced by Oxidative Stress

Cited by 61 publications

References 52 publications

Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis

Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis

Insulin-like growth factor binding protein 7 and tissue inhibitor of metalloproteinases-2: differential expression and secretion in human kidney tubule cells

Receptor role of the annexin A2 in the mesothelial endocytosis of crocidolite fibers

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