Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells

Mercer, Natalia; Ahmed, Hafiz; Etcheverry, Susana B.; Vasta, Gerardo R.; Cortizo, Ana Marı́a

doi:10.1007/s11010-007-9557-8

Cited by 79 publications

(73 citation statements)

References 24 publications

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“…In the nucleus, STAT3 binds to target genes and induces the transcription of several genes associated with cell proliferation and anti-apoptosis [48, 49]. We have been working on the gene regulation and functional characterization of galectin-3 over the years [16, 31, 46, 54–56]. Several studies suggest that galectin-3 is involved in tumor cell adhesion, proliferation, angiogenesis, cancer progression and metastasis [13, 16–20].…”

Section: Discussionmentioning

confidence: 99%

Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Guha

Bandyopadhyaya

Polumuri

et al. 2014

Breast Cancer Res Treat

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Nicotine, a main addictive compound in tobacco smoke, has been linked to promotion and progression of lung, head and neck, pancreatic, and breast cancers, but the detailed mechanisms of cancer progression remain elusive. Here we show that nicotine induces the expression of galectin-3 (an anti-apoptotic β-galactoside-binding lectin) in breast cancer cell line and in primary tumors from breast cancer patients. Nicotine-induced up regulation of galectin-3 is due to an increased expression of α9 isoform of nicotinic acetylcholine receptor (α9nAChR), which activates transcription factor STAT3 that in turn, physically binds to galectin-3 (LGALS3) promoter and induces transcription of galectin-3. Intracellular galectin-3 increased mitochondrial integrity and suppressed chemotherapeutic-induced apoptosis of breast cancer cell. Moreover, nicotine induced enrichment of side population cells with cancer stem cell-like properties was modulated by galectin-3 expression and could be significantly reduced by transient knock down of LGALS3 and its upstream signaling molecules STAT3 and α9nAChR. Thus, galectin-3 or its upstream signaling molecule STAT3 or α9nAChR could be a potential target to prevent nicotine-induced chemoresistance in breast cancer.

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Section: Discussionmentioning

confidence: 99%

Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Guha

Bandyopadhyaya

Polumuri

et al. 2014

Breast Cancer Res Treat

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“…In contrast, non-cross-linking types of AGEs, such as carboxymethyllysine, deteriorate osteoblastic function [86,87] via interaction with the cell surface receptor of AGEs, receptor for advanced glycosylation end products (RAGE) [88]. Such adverse effects of AGEs on osteoblastic function are also reported by Pen itself [89].…”

Section: Lysyl Oxidase and Total Enzymatic Cross-link Formationmentioning

confidence: 99%

Collagen cross-links as a determinant of bone quality: a possible explanation for bone fragility in aging, osteoporosis, and diabetes mellitus

2009

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Collagen cross-linking, a major post-translational modification of collagen, plays important roles in the biological and biomechanical features of bone. Collagen cross-links can be divided into lysyl hydroxylase and lysyloxidase-mediated enzymatic immature divalent cross-links,mature trivalent pyridinoline and pyrrole cross-links, and glycation- or oxidation-induced non-enzymatic cross-links(advanced glycation end products) such as glucosepane and pentosidine. These types of cross-links differ in the mechanism of formation and in function. Material properties of newly synthesized collagen matrix may differ in tissue maturity and senescence from older matrix in terms of crosslink formation. Additionally, newly synthesized matrix in osteoporotic patients or diabetic patients may not necessarily be as well-made as age-matched healthy subjects. Data have accumulated that collagen cross-link formation affects not only the mineralization process but also microdamage formation. Consequently, collagen cross-linking is thought to affect the mechanical properties of bone. Furthermore,recent basic and clinical investigations of collagen cross-links seem to face a new era. For instance, serum or urine pentosidine levels are now being used to estimate future fracture risk in osteoporosis and diabetes. In this review, we describe age-related changes in collagen cross-links in bone and abnormalities of cross-links in osteoporosis and diabetes that have been reported in the literature.

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“…AGEs have a physiological function and act through their receptors. It has been shown that receptor for AGEs (RAGE) is expressed in osteoblasts and osteocytes [25,26], and hyperglycemia increased the expression of RAGE [27]. We previously demonstrated that combination of high glucose and AGEs inhibited the mineralization of osteoblastic MC3T3-E1 cells [27], and that AGEs inhibited the osteoblastic differentiation or mineralization of mouse stromal ST2 cells and human mesenchymal stem cells by decreasing osterix expression, increasing transforming growth factor (TGF)-β expression, and suppressing endoplasmic reticulum stress proteins [28][29][30] (Fig.…”

Section: Dysfunction Of Osteoblastsmentioning

confidence: 99%

Interaction between bone and glucose metabolism [Review]

Kanazawa

2017

Endocr J

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Abstract.Accumulating evidence has shown that bone and glucose metabolism are closely associated with each other. Since the risk of osteoporotic fractures is increased in patients with diabetes mellitus (DM), osteoporosis is recently recognized as one of diabetic complications, called DM-induced bone fragility. Previous studies showed that collagen cross-links of advanced glycation end products (AGEs) and dysfunctions of osteoblast and osteocyte are involved in DMinduced bone fragility. Circulating levels of AGEs and homocysteine are increased in patients with DM, and they directly impair the functions of osteoblast and osteocyte, resulting in decreased bone formation and bone remodeling. On the other hand, bone is recently recognized as an endocrine organ. Previous studies based on in vitro and animal studies showed that osteocalcin, which is specifically expressed in osteoblasts and secreted into the circulation, may regulate glucose homeostasis. Although several clinical studies reported the relationship between osteocalcin and glucose metabolism, further large-scale and intervention studies are necessary to confirm the beneficial effects of osteocalcin on glucose metabolism in human. It has been shown that adenosine monophosphate-activated protein kinase (AMPK), an intracellular energy sensor, is involved in bone metabolism. Adiponectin and metformin stimulate osteocalcin expression and the differentiation of osteoblasts via AMPK activation. Also, AMPK activation protects against oxidative stress-induced apoptosis of osteocytes. These findings suggest that AMPK in osteoblasts and osteocytes may be a therapeutic target for DM-induced bone fragility.

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Regulation of advanced glycation end product (AGE) receptors and apoptosis by AGEs in osteoblast-like cells

Cited by 79 publications

References 24 publications

Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Nicotine promotes apoptosis resistance of breast cancer cells and enrichment of side population cells with cancer stem cell-like properties via a signaling cascade involving galectin-3, α9 nicotinic acetylcholine receptor and STAT3

Collagen cross-links as a determinant of bone quality: a possible explanation for bone fragility in aging, osteoporosis, and diabetes mellitus

Interaction between bone and glucose metabolism [Review]

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