Glucose Deprivation Increases mRNA Stability of Vascular Endothelial Growth Factor through Activation of AMP-activated Protein Kinase in DU145 Prostate Carcinoma

Hu, Yun; Lee, Minyoung; Kim, Sung‐Soo; Ha, Joohun

doi:10.1074/jbc.m412994200

Cited by 137 publications

(107 citation statements)

References 42 publications

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“…We are now focusing on identifying how glucose concentration regulates AM mRNA expression. Our preliminary data suggest that AMPK is implicated in the regulation of AM mRNA expression by glucose concentration (data not shown), in accordance with previous reports, 10,11 and that stability of AM mRNA may not be involved in this regulation, in contrast to a previous report. 12 Tumor cells were implanted s.c. in the back of SCID mice and grown to B5 mm in diameter.…”

Section: Resultssupporting

confidence: 92%

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

et al. 2006

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We have recently reported that the intra-tumoral injection of adrenomedullin (AM) antagonist (AMA; AM (22-52)) peptides significantly reduced the in vivo growth of a pancreatic cancer cell line in severely combined immunodeficient (SCID) mice. In the present study, we examined the effects of intra-tumoral and intra-muscular transfers of naked DNA encoding AMA on the in vivo growth of cancer cell lines. We demonstrate that these treatments induce the regression of a pancreatic cancer cell line and a breast cancer cell line inoculated in SCID mice. Furthermore, CD31-positive cells disappear completely from tumor tissues, following treatment, indicating that neo-vascularization is entirely inhibited. These results suggest that the intra-tumoral or intra-muscular transfer of naked DNA encoding AMA might be a promising alternative modality for treating human cancers.

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Section: Resultssupporting

confidence: 92%

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

et al. 2006

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“…In relation to the latter assumption, we have observed that long-term activation of AMPK in rat Sertoli cells increases GLUT1 expression suggesting that this protein is essential for Sertoli cell functioning. The close relationship between AMPK and GLUT1 expression has been previously documented in skeletal muscle cells transfected with a constitutively active mutant form of the catalytic a-subunit of AMPK and in DU145 prostate carcinoma cells stimulated with AICAR (Fryer et al 2002, Yun et al 2005. On the other hand, the decrease in GLUT3 mRNA levels following long-term activation of AMPK can be readily explained by the general inhibitory effect of AMPK activation on anabolic processes (Corton et al 1994).…”

Section: Discussionmentioning

confidence: 90%

The AMP-activated protein kinase activator, 5-aminoimidazole-4-carboxamide-1-b-d-ribonucleoside, regulates lactate production in rat Sertoli cells

Galardo¹,

Riera²,

Pellizzari³

et al. 2007

Journal of Molecular Endocrinology

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The aim of the present study was to investigate whether the AMP-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis, is present in Sertoli cells and whether its activation by 5-aminoimidazole-4-carboxamide-1-b-Dribonucleoside (AICAR) results in the regulation of cell metabolism to ensure lactate supply for germ cell development. Sertoli cell cultures from 20-day-old rats were used. Western blot analysis for the a-subunit of AMPK showed that high levels of AMPK are present in Sertoli cells. Treatment of the cultures with AICAR resulted in a dose-and time-dependent increase of P-AMPK levels indicating activation of the enzyme. A possible effect of AICAR on Sertoli cell lactate production was then analyzed. A dose-and time-dependent increment in lactate secretion was observed. The participation of AMPK activation in different biochemical processes that may be implicated in the regulation of lactate production was also analyzed. AICAR stimulated glucose uptake in a dose-and time-dependent manner. Additionally, AICAR increased the glucose transporter 1 (GLUT1) and decreased the glucose transporter 3 (GLUT3) mRNA levels. As for the role of AMPK in the regulation of the monocarboxylate transporters 1 and 4 (MCT1 and MCT4), it has been observed that AICAR treatment decreased MCT1 and increased MCT4 mRNA levels. In summary, the results presented herein show that AMPK is present in Sertoli cells and that its activation by AICAR increases lactate production as a result, at least in part, of a) an increase in glucose uptake, b) an increase in GLUT1 expression, and c) a decrease in MCT1 and an increase in MCT4 levels. Altogether, these results suggest an important role of AMPK in modulating the nutritional function of Sertoli cells.

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“…The first occurred when DU145 PCa cells were subjected to glucose deprivation. Under these conditions, VEGF transcript stability was increased as a result of the stimulation of AMP-activated protein kinase through a mechanism that is still unknown (Yun et al 2005). In addition to this, an isoform of the Wilms' tumor suppressor gene (WT1-A) was found to modestly increase VEGF transcript stability in a hormone-enhanced mechanism when WT1 was stably overexpressed in LNCaP PCa cells.…”

Section: Post-transcriptional Regulation Of Vegf Signaling In Pcamentioning

confidence: 85%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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Glucose Deprivation Increases mRNA Stability of Vascular Endothelial Growth Factor through Activation of AMP-activated Protein Kinase in DU145 Prostate Carcinoma

Cited by 137 publications

References 42 publications

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

Suppression of tumor growth by intra-muscular transfer of naked DNA encoding adrenomedullin antagonist

The AMP-activated protein kinase activator, 5-aminoimidazole-4-carboxamide-1-b-d-ribonucleoside, regulates lactate production in rat Sertoli cells

Regulation of vascular endothelial growth factor in prostate cancer

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