Curcumin suppresses HIF1A synthesis and VEGFA release in pituitary adenomas

Shan, Bing; Schaaf, Christian; Schmidt, Anne W.; Lucia, K.; Buchfelder, Michael; Losa, Marco; Kuhlen, Dominique; Kreutzer, Jürgen; Perone, Marcelo J.; Arzt, Eduardo; Stalla, Günter; Renner, Ulrich

doi:10.1530/joe-12-0207

Cited by 47 publications

(32 citation statements)

References 55 publications

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“…An important contributor to tumors propensity to invade and metastasize is angiogenesis. Cell lines derived from surgically resected pituitary adenomas treated with curcumin have decreased HIF1A and VEGFA, both of which are involved in tumoral angiogenesis [56]. …”

Section: Mechanism and Preclinical Datamentioning

confidence: 99%

Therapeutic Potential of Curcumin for the Treatment of Brain Tumors

Klinger

Mittal

2016

Oxidative Medicine and Cellular Longevity

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Brain malignancies currently carry a poor prognosis despite the current multimodal standard of care that includes surgical resection and adjuvant chemotherapy and radiation. As new therapies are desperately needed, naturally occurring chemical compounds have been studied for their potential chemotherapeutic benefits and low toxicity profile. Curcumin, found in the rhizome of turmeric, has extensive therapeutic promise via its antioxidant, anti-inflammatory, and antiproliferative properties. Preclinical in vitro and in vivo data have shown it to be an effective treatment for brain tumors including glioblastoma multiforme. These effects are potentiated by curcumin's ability to induce G2/M cell cycle arrest, activation of apoptotic pathways, induction of autophagy, disruption of molecular signaling, inhibition of invasion, and metastasis and by increasing the efficacy of existing chemotherapeutics. Further, clinical data suggest that it has low toxicity in humans even at large doses. Curcumin is a promising nutraceutical compound that should be evaluated in clinical trials for the treatment of human brain tumors.

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Section: Mechanism and Preclinical Datamentioning

confidence: 99%

Therapeutic Potential of Curcumin for the Treatment of Brain Tumors

Klinger

Mittal

2016

Oxidative Medicine and Cellular Longevity

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“…Previous research from Shan found that curcumin inhibits the synthesis of hypoxia-induced mRNA and secretion from VEGFA in GH3 cells and the culture of pituitary adenoma cells in humans supports the suppressive effect on neovascularization of pituitary tumors (25). Several other cancer studies have also stated that curcumin suppresses VEGF expression in Ehrlich tumor ascites cells and NIH3T3 cells (26), in pancreatic tumors (16), and in ovarian cancer (27).…”

Section: Discussionmentioning

confidence: 85%

Effects of Curcumin on Vascular Endothelial Growth Factor Expression on Rattus norvegicus Cervical Cancer Xenograft Model

Muninggar

Widjiati

Yuliati

et al. 2019

Indonesian Journal of Cancer

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Objective: To analyze the effect of curcumin in VEGF expression on Rattus norvegicus cervical cancer cell xenograft model.Methods: An experimental study with randomized post test only control group design. The subjects were Rattus norvegicus (Sprague Dawley), inoculated with He-la cervical cancer cells from American Type Culture Collection (ATCC) processed in stem cell laboratory Institute of Tropical Disease (ITD) Airlangga University. 5x106 of He-La cells were injected subcutaneously in dorsal flank area of Rattus norvegicus. After 30 days of observation we performed histopathological examination of xenograft tissue and randomized into 2 groups which were given curcumin orally 1000 mg/kg (curcumin group) vs. no therapy (control group). After another 30 days the xenograft tissue was dissected and underwent immunochemistry examination for VEGF expression.Results: 32 samples of Rattus norvegicus were divided into 2 groups, In curcumin group the VEGF median expression was 2,2 (0,3-7,6) and in control group the VEGF median expression was 6,6 (1,2-12). There was a statistically significant difference with p value =0,009 with Mann Whitney test (p<0,05).Conclusion: VEGF expression in Rattus norvegicus xenograft model of cervical cancer was suppressed by giving Curcumin 1000 mg/kgBB orally.

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“…The present study shows that in vivo inhibition of the NF-jB pathway not only reduced cell proliferation, but also increased apoptosis in GH3 tumours growing in nude mice. NFjB inhibitors were suggested to reduce tumour progression by their suppressive effects on tumour neovascularisation (47,48). Therefore, we cannot rule out that the effect of BAY on GH3 cell turnover in vivo is additionally mediated through other mechanisms (i.e.…”

Section: Discussionmentioning

confidence: 97%

Lack of Oestrogenic Inhibition of the Nuclear Factor‐κB Pathway in Somatolactotroph Tumour Cells

Eijo

Gottardo

Jaita

et al. 2015

J Neuroendocrinology

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Activation of nuclear factor (NF)-κB promotes cell proliferation and inhibits apoptosis. We have previously shown that oestrogens sensitise normal anterior pituitary cells to the apoptotic effect of tumour necrosis factor (TNF)-α by inhibiting NF-κB nuclear translocation. In the present study, we examined whether oestrogens also modulate the NF-κB signalling pathway and apoptosis in GH3 cells, a rat somatolactotroph tumour cell line. As determined by Western blotting, 17β-oestradiol (E2 ) (10(-9) m) increased the nuclear concentration of NF-κB/p105, p65 and p50 in GH3 cells. However, E2 did not modify the expression of Bcl-xL, a NF-κB target gene. TNF-α induced apoptosis of GH3 cells incubated in either the presence or absence of E2 . Inhibition of the NF-kB pathway using BAY 11-7082 (BAY) (5 μm) decreased the viability of GH3 cells and increased the percentage of terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL)-positive GH3 cells. BAY also increased TNF-α-induced apoptosis of GH3 cells, an effect that was further increased by an inhibitor of the c-Jun N-terminal protein kinase pathway, SP600125 (10 μm). We also analysed the role of the NF-κB signalling pathway on proliferation and apoptosis of GH3 tumours in vivo. The administration of BAY to nude mice bearing GH3 tumours increased the number of TUNEL-positive cells and decreased the number of proliferating GH3 cells. These findings suggest that GH3 cells lose their oestrogenic inhibitory action on the NF-κB pathway and that the pro-apoptotic effect of TNF-α on these tumour pituitary cells does not require sensitisation by oestrogens as occurs in normal pituitary cells. NF-κB was required for the survival of GH3 cells, suggesting that pharmacological inhibition of the NF-κB pathway could interfere with pituitary tumour progression.

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Curcumin suppresses HIF1A synthesis and VEGFA release in pituitary adenomas

Cited by 47 publications

References 55 publications

Therapeutic Potential of Curcumin for the Treatment of Brain Tumors

Therapeutic Potential of Curcumin for the Treatment of Brain Tumors

Effects of Curcumin on Vascular Endothelial Growth Factor Expression on Rattus norvegicus Cervical Cancer Xenograft Model

Lack of Oestrogenic Inhibition of the Nuclear Factor‐κB Pathway in Somatolactotroph Tumour Cells

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