The role of VEGF and a functional link between VEGF and p27Kip1 in acute myeloid leukemia

Węgiel, Barbara; Ekberg, Jenny; Talasila, Krishna M.; Jalili, S; Persson, Jenny L.

doi:10.1038/leu.2008.300

Cited by 28 publications

(20 citation statements)

References 35 publications

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“…According to the results, its serum levels, as well as its cytoplasmic expression in bone marrow blasts, were associated with chemotherapy outcome, a finding which is again in consistence with VEGF’s reported role in leukemia-associated angiogenesis 42. This rapidly expanding research activity surrounding endocan is facilitated by the relatively simple laboratory methods developed for such purposes, including sandwich enzyme-linked immunosorbent assays, immunohistochemistry and immunoprecipitation.…”

Section: Endocan: General Knowledgementioning

confidence: 83%

Endocan and the respiratory system: a review

Kechagia¹,

Papassotiriou²,

Gourgoulianis³

2016

COPD

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Endocan, formerly called endothelial cell-specific molecule 1, is an endothelial cell-associated proteoglycan that is preferentially expressed by renal and pulmonary endothelium. It is upregulated by proangiogenic molecules as well as by pro-inflammatory cytokines, and since it reflects endothelial activation and dysfunction, it is regarded as a novel tissue and blood-based relevant biomarker. As such, it is increasingly being researched and evaluated in a wide spectrum of healthy and disease pathophysiological processes. Here, we review the present scientific knowledge on endocan, with emphasis on the evidence that underlines its possible clinical value as a prognostic marker in several malignant, inflammatory and obstructive disorders of the respiratory system.

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Section: Endocan: General Knowledgementioning

confidence: 83%

Endocan and the respiratory system: a review

Kechagia¹,

Papassotiriou²,

Gourgoulianis³

2016

COPD

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“…Vascular endothelial growth factor (VEGF) is expressed in normal breast and uterine cells and its expression is regulated by ER-α in response to estrogen stimuli [4–7]. VEGF, a key factor in angiogenesis has been shown to promote tumor growth, invasion and distant metastasis in several cancer types such as leukemia and breast cancer [8–10]. The autocrine and paracrine signalling mediated by VEGF and its receptors contribute to the increased proliferation and survival of breast cancer cells [11–13].…”

Section: Introductionmentioning

confidence: 99%

Cyclin A1 Modulates the Expression of Vascular Endothelial Growth Factor and Promotes Hormone-Dependent Growth and Angiogenesis of Breast Cancer

et al. 2013

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Alterations in cellular pathways related to both endocrine and vascular endothelial growth factors (VEGF) may contribute to breast cancer progression. Inhibition of the elevated levels of these pathways is associated with clinical benefits. However, molecular mechanisms by which endocrine-related pathways and VEGF signalling cooperatively promote breast cancer progression remain poorly understood. In the present study, we show that the A-type cyclin, cyclin A1, known for its important role in the initiation of leukemia and prostate cancer metastasis, is highly expressed in primary breast cancer specimens and metastatic lesions, in contrasting to its barely detectable expression in normal human breast tissues. There is a statistically significant correlation between cyclin A1 and VEGF expression in breast cancer specimens from two patient cohorts (p<0.01). Induction of cyclin A1 overexpression in breast cancer cell line MCF-7 results in an enhanced invasiveness and a concomitant increase in VEGF expression. In addition, there is a formation of protein–protein complexes between cyclin A1 and estrogen receptor ER-α cyclin A1 overexpression increases ER-α expression in MCF-7 and T47D cells. In mouse tumor xenograft models in which mice were implanted with MCF-7 cells that overexpressed cyclin A1 or control vector, cyclin A1 overexpression results in an increase in tumor growth and angiogenesis, which is coincident with an enhanced expression of VEGF, VEGFR1 and ER-α Our findings unravel a novel role for cyclin A1 in growth and progression of breast cancer, and suggest that multiple cellular pathways, including cell cycle regulators, angiogenesis and estrogen receptor signalling, may cooperatively contribute to breast cancer progression.

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“…The inhibition of CHK2 was earlier reported to sensitize malignant cells to apoptosis 31 . Also, the VEGFR1 was known to be a potential target in leukemia and other cancer forms, and the inhibition of VEGFR1 reported to induce apoptosis in leukemia cells32, 33, 34. This is because the VEGF acts as a growth factor in leukemic cells like MOLT-4, and cells express VEGFR1 receptors on their cell surfaces 33 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of protein kinases by anticancer DNA intercalator, 4-butylaminopyrimido[4′,5′:4,5]thieno(2,3- b )quinoline

Kumar

et al. 2017

Acta Pharmaceutica Sinica B

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Targeting protein kinases (PKs) has been a promising strategy in treating cancer, as PKs are key regulators of cell survival and proliferation. Here in this study, we studied the ability of pyrimido[4′,5′:4,5]thieno(2,3-b)quinolines (PTQ) to inhibit different PKs by performing computational docking and in vitro screening. Docking studies revealed that 4-butylaminopyrimido[4′,5′:4,5]thieno(2,3-b)quinoline (BPTQ) has a higher order of interaction with the kinase receptors than other PTQ derivatives. In vitro screening confirms that BPTQ inhibits VEGFR1 and CHK2, with the IC50 values of 0.54 and 1.70 µmol/L, respectively. Further, cytotoxicity of BPTQ was measured by trypan blue assay. Treatment with BPTQ decreased the proliferation of HL-60 cells with an IC50 value of 12 µmol/L and induces apoptosis, as explicated by the fall in the mitochondrial membrane potential, annexin V labeling and increased expression of caspase-3. Taken together, these data suggest that BPTQ possess ability to inhibit PKs and to induce cell death in human promyelocytic leukemia cells.

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The role of VEGF and a functional link between VEGF and p27Kip1 in acute myeloid leukemia

Cited by 28 publications

References 35 publications

Endocan and the respiratory system: a review

Endocan and the respiratory system: a review

Cyclin A1 Modulates the Expression of Vascular Endothelial Growth Factor and Promotes Hormone-Dependent Growth and Angiogenesis of Breast Cancer

Inhibition of protein kinases by anticancer DNA intercalator, 4-butylaminopyrimido[4′,5′:4,5]thieno(2,3- b )quinoline

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