Gambogic acid inhibits the growth of ovarian cancer tumors by regulating p65 activity

Tang, Qiusha; Lu, Mengji; Zhou, Huan; Chen, Daozhen; Liu, Lu

doi:10.3892/ol.2016.5433

Cited by 26 publications

(14 citation statements)

References 24 publications

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“…And we also found that treatment with gambogic acid significantly suppressed NF-κB and MMP-2 and MMP-9 protein expression in RA mice. Tang et al (11) suggested that gambogic acid inhibits the growth of ovarian cancer tumors through RELA/NF-κB p65 (p65) activity. Qi et al (22) indicated that gambogic acid suppressed lung metastasis of human breast carcinoma cell through protein kinase C (PKC) mediated MMP-2/9 expression inhibition.…”

Section: Discussionmentioning

confidence: 99%

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Anti‑inflammatory effects of gambogic acid in murine collagen‑induced arthritis through PI3K/Akt signaling pathway

Wang

Yang

2018

Mol Med Report

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Garcinia angustifolia is a dry resin secreted by Garcinia cambogia, which has the functions of breaking blood, detoxifying, stopping bleeding and killing insects. It is used for the treatment of cancer and brain edema. Gambogic acid is the primary active ingredient. The present study aimed to investigate the anti‑inflammatory and antiproliferative effects of gambogic acid on arthritis and the possible mechanisms. It was demonstrated that gambogic acid decreased arthritic scores in murine collagen‑induced arthritic mice. The tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 concentrations, and caspase‑3 and caspase‑9 were significantly inhibited by gambogic acid in arthritic mice. Gambogic acid decreased matrix metalloproteinases (MMP)‑2, MMP‑9, nuclear factor (NF)‑κB and phosphorylated‑p38 protein expression, and increased tissue inhibitors of matrix metalloproteases‑1 (TIMP‑1) protein expression in arthritic mice. Furthermore, the phosphoinositide 3‑kinase (PI3K)/AKT serine/threonine kinase (Akt) signaling pathway was induced in arthritic mice treated with gambogic acid. The results suggested that gambogic acid induced anti‑inflammatory effects in murine collagen‑induced arthritis, through the PI3K/Akt signaling pathway, and offers future potential for application in arthritis patients.

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Section: Discussionmentioning

confidence: 99%

“…Gambogic acid ( Fig. 1) has anti-inflammatory, antioxidation and anticancer effects (11,12). Ma et al (13) showed that gambogic acid inhibits osteoclast formation and ovariectomy-induced osteoporosis.…”

Section: Introductionmentioning

confidence: 99%

Anti‑inflammatory effects of gambogic acid in murine collagen‑induced arthritis through PI3K/Akt signaling pathway

Wang

Yang

2018

Mol Med Report

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“…NF-κB p65 is a well-recognized anti-apoptotic transcription factor and abnormal expression or activation of NF-κB p65 has been found in multiple types of malignant cancers such as cervical cancer, esophageal squamous cancer, ovarian cancer, breast cancer and glioma et al [13,[26][27][28][29]. NF-κB promotes tumorigenesis and therapy resistance mainly through induction of master transcription factors including signal transducer and activator of transcription 3 (STAT3) and TAZ [30].…”

Section: Discussionmentioning

confidence: 99%

Nuclear Factor I A Promotes Temozolomide Resistance in Glioblastoma via Transcriptional Regulation of Nuclear Factor κB Pathway

Wang

Zuo

et al. 2019

Preprint

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Background: Glioma is one of the most common primary brain tumors in human with severe mortality based on its therapy resistance and recurrence. Many molecular pathways and regulation factors have been proved to be required for GBM growth and therapy resistance, however, the underlying molecular mechanisms still remains unclear. Methods: Nuclear factor I-A (NFIA) was identified as a key candidate kinase encoding gene in chemoresistance regulation by using kinome-wide bioinformatic analysis. Afterwards, the potential biological functions of NFIA in oncogenesis and chemoresistance were clarified by qRT-PCR, western blotting and in vivo xenograft models followed by temozolomide (TMZ) resistant U87 cell induction. Additionally, immunohistochemistry (IHC) assays were performed to explore the clinical significance of AURKB in glioma patients. At last, lentiviral silencing of NFIA was used to explore the potential downstream targets for NFIA in acquired TMZ resistance in GBM.. Results: We identified NFIA was the most correlated gene for TMZ resistance in GBM. Clinically, elevated NFIA expression was significantly correlated to adverse outcomes of glioma patients especially in GBM patients. Moreover, NFIA was functionally required for TMZ resistance of U87 cells while suppression of NFIA via lentivirus infection reduced cell proliferation, tumorigenesis as well as resistance to TMZ in GBM cells. Lastly, NFIA promoted acquired TMZ resistance in GBM via transcription activity thus regulated the expression of nuclear factor κB (NF-kB). Conclusions: Altogether, our study suggests that NFIA-dependent transcriptional regulation of NF-kB contributes to the acquired TMZ resistance in GBM, indicating that NFIA-NF-κB axis could be a new therapeutic target for TMZ resistant GBM.

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“…In line with previous studies, our data demonstrated that TKL can strongly inhibit the phosphorylation of IKKβ and IκBα, and subsequently reduce the nuclear translocation of NF-κB p65 (p65). In addition, p65 might also regulate the expression of several genes involved in apoptosis, mainly through its tight binding to the CASP9 gene, and subsequent influence on caspase-9 expression [ 37 , 38 ]. We propose that p65/caspase-9 signals may be attractive targets for treating DN, due to their pro-apoptotic activity.…”

Section: Discussionmentioning

confidence: 99%

Trichosanthes kirilowii lectin alleviates diabetic nephropathy by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway

Peng

Xiang

et al. 2018

Bioscience Reports

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Trichosanthes kirilowii lectin (TKL) has been reported to exert hypoglycemic effects in alloxan-induced diabetic mice. However, there is no evidence showing that it helps to prevent diabetic nephropathy (DN). We used a high glucose (HG)-induced HK-2 cell model and a streptozocin (STZ)-induced Wistar rat model to investigate the effects of TKL on DN, as well as the mechanisms for those effects. Our results showed that TKL significantly increased the viability of HG-treated HK-2 cells and inhibited cell apoptosis. In vivo experiments demonstrated that TKL attenuated STZ-induced histopathological damage and the inflammatory response in rat kidney tissues. Pre-treatment of HK-2 cells or STZ-treated rats with polyinosinic acid (Poly IC), an inhibitor of lectin-like oxLDL receptor 1 (LOX1), blocked the protective effect of TKL against HG- or STZ-induced damage to kidney tissue, indicating that TKL might exert its effect via LOX1-mediated endocytosis. Additional results suggested that TKL inhibits the phosphorylation of IκB kinase β (IKKβ) and the nuclear factor-κB (NF-κB) inhibitor protein (IκBα), and thereby reduces the nuclear translocation of NF-κB (p65). ChIP assay data indicated that TKL markedly inhibits the binding of p65 to the CASP9 gene in HG-treated HK-2 cells, subsequently suppressing transcription of the CASP9 gene. In the dual-luciferase reporter assay, TKL significantly inhibited luciferase activity in cells co-transfected with p65 and a wild-type capase-9 construct instead of mutated caspase-9 constructs.Taken together, our results show that TKL helps to protect against DN by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway, suggesting TKL as a promising agent for treating DN.

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Gambogic acid inhibits the growth of ovarian cancer tumors by regulating p65 activity

Cited by 26 publications

References 24 publications

Anti‑inflammatory effects of gambogic acid in murine collagen‑induced arthritis through PI3K/Akt signaling pathway

Anti‑inflammatory effects of gambogic acid in murine collagen‑induced arthritis through PI3K/Akt signaling pathway

Nuclear Factor I A Promotes Temozolomide Resistance in Glioblastoma via Transcriptional Regulation of Nuclear Factor κB Pathway

Trichosanthes kirilowii lectin alleviates diabetic nephropathy by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway

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