Serum Vascular Endothelial Growth Factor and Adiponectin Levels in Patients With Benign and Malignant Gynecological Diseases

Lasalandra, Carla; Coviello, M.; Falco, Gaetano; Divella, Rosa; Trojano, Giuseppe; Laterza, Anna Maria; Quero, Carmela; Pepe, Vito; Zito, Francesco Alfredo; Quaranta, Michele

doi:10.1111/igc.0b013e3181c54fc5

Cited by 8 publications

(10 citation statements)

References 26 publications

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“…COX-2 inhibitors suppress the expression and secretion of MMP-2 and-9, suggesting that COX-2 also promotes tumour angiogenesis and tumour invasion. Furthermore, it was also reported that the downstream products of COX-2 stimulate VEGF to promote angiogenesis 30 . Taken together, our studies suggest that the decrease in angiogenesis by DATS may be due to the reduction in COX-2, VEGF which leads to the inhibition of MMP-2, -7 and -9 and inhibition of migration and invasion (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…A) in HT‐29 cells. It was reported that the overexpression of COX‐II is associated with the initiation of angiogenesis and COX‐2 inhibitors can block angiogenesis . COX‐2 inhibitors suppress the expression and secretion of MMP‐2 and‐9, suggesting that COX‐2 also promotes tumour angiogenesis and tumour invasion.…”

Section: Discussionmentioning

confidence: 99%

“…All samples were assayed for VEGF concentrations by ELISA assay kits (R&D Systems, Minneapolis, MN, USA) that were used according to the manufacturer's recommendations. Absorbance was monitored at 450 nm with a reference wavelength of 570 nm with an ELISA reader .…”

Section: Methodsmentioning

confidence: 99%

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Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth

Lai

Hsu

Yang

et al. 2014

J Cellular Molecular Medi

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Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis-dependent diseases including cancer. We examined the cytotoxic, anti-metastatic, anti-cancer and anti-angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases-2, -7 and -9 and VEGF. In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras. DATS also inhibited the secretion of VEGF. The capillary-like tube structure formation and migration by HUVEC was inhibited by DATS. The chicken egg chorioallantoic membrane (CAM) assay indicated that DATS treatment inhibited ex-vivo angiogenesis. We investigated the anti-tumour effects of DATS against human colon cancer xenografts in BALB/cnu/nu mice and its anti-angiogenic activity in vivo. In this in-vivo study, DATS also inhibited the tumour growth, tumour weight and angiogenesis (decreased the levels of haemoglobin) in HT29 cells. In conclusion, the present results suggest that the inhibition of angiogenesis may be an important mechanism in colon cancer chemotherapy by DATS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth

Lai

Hsu

Yang

et al. 2014

J Cellular Molecular Medi

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“…2004, Ashizawa et al . 2010, Lasalandra et al . 2010) that measured adiponectin found evidence for an association with endometrial cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Case–control study of markers of insulin resistance and endometrial cancer risk

Friedenreich¹,

Langley²,

Speidel³

et al. 2012

Endocrine-Related Cancer

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Markers of insulin resistance such as the adiponectin:leptin ratio (A:L) and the homeostasis model assessment ratio (HOMA-IR) are associated with obesity and hyperinsulinemia, both established risk factors for endometrial cancer, and may therefore be informative regarding endometrial cancer risk. This study investigated the association between endometrial cancer risk and markers of insulin resistance, namely adiponectin, leptin, the A:L ratio, insulin, fasting glucose, and the HOMA-IR. We analyzed data from 541 incident endometrial cancer cases and 961 frequency age-matched controls in a population-based case–control study in Alberta, Canada from 2002 to 2006. Participants completed interview-administered questionnaires were assessed for anthropometric measures, and provided 8-h fasting blood samples either pre- or postoperatively. Blood was analyzed for concentrations of leptin, adiponectin, and insulin by immunoassay, and fasting plasma glucose levels were determined by fluorimetric quantitative determination. Compared with the lowest quartile, the highest quartile of insulin and HOMA-IR was associated with 64% (95% confidence intervals (CI): 1.12–2.40) and 72% (95% CI: 1.17–2.53) increased risks of endometrial cancer, respectively, and the highest quartile of adiponectin was associated with a 45% (95% CI: 0.37–0.80) decreased risk after multivariable adjustments. Null associations were observed between fasting glucose, leptin and A:L, and endometrial cancer risk. This population-based study provides evidence for a role of insulin resistance in endometrial cancer etiology and may provide one possible pathway whereby obesity increases the risk of this common cancer. Interventions aimed at decreasing both obesity and insulin resistance may decrease endometrial cancer risk.

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“…[ 41 ] Furthermore, evidence suggested that the inflammatory cytokine of COX-2 could promote tumor angiogenesis and tumor invasion, and the downregulation of COX-2 inhibited cancer metastasis through preventing migration and invasion. [ 42 43 ] IL-6, linking the relationship between inflammation and cancer, was an indispensable inflammatory cytokines for cancer cell proliferation and invasion. [ 44 45 ] In the present study, we demonstrated that the levels of inflammation factors of TNF-α, COX-2, and IL-6 in cell supernatant were suppressed by quercetin in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Quercetin suppresses the migration and invasion in human colon cancer Caco-2 cells through regulating toll-like receptor 4/Nuclear Factor-kappa B pathway

2016

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Objective:The migration and invasion features, which were associated with inflammatory response, acted as vital roles in the development of colon cancer. Quercetin, a bioflavonoid compound, was widely spread in vegetables and fruits. Although quercetin exerts antioxidant and anticancer activities, the molecular signaling pathways in human colon cancer cells remain unclear. Hence, the present study was conducted to investigate the suppression of quercetin on migratory and invasive activity of colon cancer and the underlying mechanism.Materials and Methods:The effect of quercetin on cell viability, migration, and invasion of Caco-2 cells was analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound-healing assay, and transwell chambers assay, respectively. The protein expressions of toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB) p65, mitochondrial membrane potential-2 (MMP-2), and MMP-9 were detected by Western blot assay. The inflammatory factors, such as tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (Cox-2), and interleukin-6 (IL-6), in cell supernatant were detected by enzyme-linked immunosorbent assay.Results:The concentration of quercetin <20 μM was chosen for further experiments. Quercetin (5 μM) could remarkably suppress the migratory and invasive capacity of Caco-2 cells. The expressions of metastasis-related proteins of MMP-2, MMP-9 were decreased, whereas the expression of E-cadherin protein was increased by quercetin in a dose-dependent manner. Interestingly, the anti-TLR4 (2 μg) antibody or pyrrolidine dithiocarbamate (PDTC; 1 μM) could affect the inhibition of quercetin on cell migration and invasion, as well as the protein expressions of MMP-2, MMP-9, E-cadherin, TLR4, and NF-κB p65. In addition, quercetin could reduce the inflammation factors production of TNF-α, Cox-2, and IL-6.Conclusion:The findings suggested for the 1st time that quercetin might exert its anticolon cancer activity via the TLR4- and/or NF-κB-mediated signaling pathway.SUMMARY Quercetin could remarkably suppress the migratory and invasive capacity of Caco-2 cellsThe expressions of metastasis-related proteins of mitochondrial membrane potential-2 (MMP-2), MMP-9 were decreased, whereas the expression of E-cadherin protein was increased by quercetin in a dose-dependent mannerThe anti-toll-like receptor 4 (TLR4) antibody or pyrrolidine dithiocarbamate affected the inhibition of quercetin on cell migration and invasion, as well as the protein expressions of MMP-2, MMP-9, E-cadherin, TLR4, and nuclear factor-kappa B p65Quercetin could reduce the inflammation factors production of tumor necrosis factors-α, cyclooxygenase-2, and interleukin-6. Abbreviations used: MTT: 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphen yltetrazolium bromide, TLR4: Toll-like receptor 4, NF-κB: Nuclear factor-kappa B, MMP-2: Mitochondrial membrane potential-2, MMP-9: Mitochondrial membrane potential-9, TNF-α: Tumor necrosis factor-α, Cox-2: Cyclooxygenase-2, IL-6: Interleukin-6, ELISA: Enzyme-linked immunosorbent assay,...

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Serum Vascular Endothelial Growth Factor and Adiponectin Levels in Patients With Benign and Malignant Gynecological Diseases

Abstract: This is one of the first report on adiponectin in benign and malignant gynecological diseases. Future studies are needed to address the clinical potential role of adiponectin in cancer.

Cited by 8 publications

References 26 publications

Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth

Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth

Case–control study of markers of insulin resistance and endometrial cancer risk

Quercetin suppresses the migration and invasion in human colon cancer Caco-2 cells through regulating toll-like receptor 4/Nuclear Factor-kappa B pathway

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