Curcumin Suppresses Tumor Growth and Angiogenesis in Human Glioma Cells Through Modulation of Vascular Endothelial Growth Factor/ Angiopoietin-2/Thrombospondin-1 Signaling

Zhang, Zhiqiang; Liu, Cong; Tan, Qijia; Xie, Caijun; Yz, Yang; Zhan, Wengang; Han, Fei; Sharma, Hari Shanker; Sharma, Aruna

doi:10.2174/1871527315666160902144513

Cited by 19 publications

(7 citation statements)

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“…Several of these compounds were previously shown to exert antitumor effects. For example, curcumin (M02 in Table 1 ) is widely used against tumors and suppresses the growth of gastric tumor cells [ 17 ] and human glioma cells [ 18 ]. Similarly, curcumol (M01) induces apoptosis in SPC-A-1 human lung adenocarcinoma cells [ 19 ], hederagenin (M06) exerts cytotoxicity in human breast and lung cancer cells [ 20 ], and demethoxycurcumin (M10) inhibits the growth of human epithelia ovarian cancer cells [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Antitumor Mechanisms of Curcumae Rhizoma Based on Network Pharmacology

Zhang

Chen

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Curcumae Rhizoma, a traditional Chinese medication, is commonly used in both traditional treatment and modern clinical care. Its anticancer effects have attracted a great deal of attention, but the mechanisms of action remain obscure. In this study, we screened for the active compounds of Curcumae Rhizoma using a drug-likeness approach. Candidate protein targets with functions related to cancer were predicted by reverse docking and then checked by manual search of the PubMed database. Potential target genes were uploaded to the GeneMANIA server and DAVID 6.8 database for analysis. Finally, compound-target, target-pathway, and compound-target-pathway networks were constructed using Cytoscape 3.3. The results revealed that the anticancer activity of Curcumae Rhizoma potentially involves 13 active compounds, 33 potential targets, and 31 signaling pathways, thus constituting a “multiple compounds, multiple targets, and multiple pathways” network corresponding to the concept of systematic actions in TCM. These findings provide an overview of the anticancer action of Curcumae Rhizoma from a network perspective, as well as setting an example for future studies of other materials used in TCM.

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Section: Discussionmentioning

confidence: 99%

Antitumor Mechanisms of Curcumae Rhizoma Based on Network Pharmacology

Zhang

Chen

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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“…However, their function can be significantly repressed by curcumin, and more effectively repressed by curcumin in combination with flavonoids, such as EGCG [185]. Such applications can lead to repression of angiogenesis via decreased VEGF production [186][187][188], blocking monocyte binding via downregulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB) signalling [189]. A model of the therapeutic effects of curcumin and flavonoids on the tumour microenvironment and tumour development is shown in Figure 2.…”

Section: Effects Of Curcumin and Flavonoids On Tumour-associated And -Infiltrating Cells: Suppression Of Ctc Supportmentioning

confidence: 99%

“…Figure 2. Simplified model of curcumin and flavonoids effects on the NSCLC microenvironment[83,119,148,158,159,162,168,170,174,175,[186][187][188][189][190][191][192][193][194][195][196]. A necessary part of igenesis and CTC spreading is the interaction of NSCLC cells with tumour-associated cells.…”

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confidence: 99%

Circulating Tumour Cells (CTCs) in NSCLC: From Prognosis to Therapy Design

et al. 2021

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Designing optimal (neo)adjuvant therapy is a crucial aspect of the treatment of non-small-cell lung carcinoma (NSCLC). Standard methods of chemotherapy, radiotherapy, and immunotherapy represent effective strategies for treatment. However, in some cases with high metastatic activity and high levels of circulating tumour cells (CTCs), the efficacy of standard treatment methods is insufficient and results in treatment failure and reduced patient survival. CTCs are seen not only as an isolated phenomenon but also a key inherent part of the formation of metastasis and a key factor in cancer death. This review discusses the impact of NSCLC therapy strategies based on a meta-analysis of clinical studies. In addition, possible therapeutic strategies for repression when standard methods fail, such as the administration of low-toxicity natural anticancer agents targeting these phenomena (curcumin and flavonoids), are also discussed. These strategies are presented in the context of key mechanisms of tumour biology with a strong influence on CTC spread and metastasis (mechanisms related to tumour-associated and -infiltrating cells, epithelial–mesenchymal transition, and migration of cancer cells).

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“…Several studies have shown the effects and mechanisms of CCM against human neuroglioma cells (19)(20)(21). CCM was shown to induce G2/M cell cycle arrest and apoptosis in U87 cells by increasing forkhead box protein O1 expression (22), and was also reported to suppress tumor growth and angiogenesis in human glioma cells through modulation of VEGF/angiopoietin-2/thrombospondin-1 signaling (23,24). Since inflammatory factors can enhance glioma growth, and CCM is an effective anti-inflammatory factor, it remains unknown whether CCM can exert its antitumor effects by inhibiting the inflammatory HSP60/TLR-4 signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

HSP60 participates in the anti‑glioma effects of curcumin

Wang

Zheng

et al. 2021

Exp Ther Med

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The chaperone protein heat shock protein 60 (HSP60) is considered a tumor promoter in several types of primary human tumors, where it orchestrates a broad range of survival programs. Curcumin (CCM) is well-established to exhibit several anticancer properties with an excellent safety profile. Our previous study showed that CCM suppresses extracellular HSP60 expression, which is typically released by activated microglia, and acts as an inflammatory factor by binding to Toll-like receptor 4 (TLR-4) on the cell membrane. The present study assessed whether CCM exerted its anti-neuroglioma effects on U87 cells via inhibition of HSP60/TLR-4 signaling, similar to that in microglia. The results demonstrated that CCM significantly inhibited the viability and invasive capacity of neuroglioma U87 cells as evidenced by a Cell Counting Kit-8 assay. Western blotting and ELISA results showed that CCM decreased the expression of HSP60 and its transcriptional factor, heat shock factor 1, and reduced HSP60 release. Accordingly, TLR-4, as the target of HSP60, and its downstream signaling proteins myeloid differentiation primary response 88 (MYD88), NF-κB, inducible nitric oxide synthase and cytokines IL-1β and IL-6 were downregulated by CCM. The expression levels of apoptotic factors associated with NF-κB activation, including TNF-α and caspase-3 were increased in U87 cells by CCM treatment, while p53 expression, a tumor suppressor, was shown to be decreased. Based on the results of the present study, CCM may exert its anti-tumor effects in U87 cells by inhibiting the HSP60/TLR-4/MYD88/NF-κB pathway and inducing tumor cell apoptosis. Thus, CCM may be used as a potential therapy for the clinical treatment of neuroglioma.

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Curcumin Suppresses Tumor Growth and Angiogenesis in Human Glioma Cells Through Modulation of Vascular Endothelial Growth Factor/ Angiopoietin-2/Thrombospondin-1 Signaling

Abstract: This study shows that curcumin inhibits tumor growth by inhibiting VEGF/Ang-2/TSP-1- mediated angiogenesis in a xenograft glioma mouse model.

Cited by 19 publications

References 0 publications

Antitumor Mechanisms of Curcumae Rhizoma Based on Network Pharmacology

Antitumor Mechanisms of Curcumae Rhizoma Based on Network Pharmacology

Circulating Tumour Cells (CTCs) in NSCLC: From Prognosis to Therapy Design

HSP60 participates in the anti‑glioma effects of curcumin

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