Curcumin suppresses colon cancer cell invasion via AMPK-induced inhibition of NF–κB, uPA activator and MMP9

Tong, Wei; Wang, Quan; Sun, Dongfa; Suo, Jian

doi:10.3892/ol.2016.5148

Cited by 114 publications

(67 citation statements)

References 52 publications

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“…NF‐κB inhibitors, which are known to regulate the NF‐κB activation stabilized by protease inhibitors, could also induce apoptosis in the human leukemia cells . A previous study has done well to demonstrate that the NF‐κB inhibitor can suppress colon cancer cell invasion through the inhibition of NF‐κB . Furthermore, our study demonstrated thoroughly that the NF‐κB inhibitor suppressed the expressions of TLR4 and NF‐κB in the serum.…”

Section: Discussionsupporting

confidence: 69%

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Zhang

Wang

Chen

et al. 2019

The Kaohsiung J of Med Scie

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The pathogenesis of acute lung injury (ALI) is characterized by lung inflammation and lung oxidative stress. The study was conducted in order to investigate the effect toll‐like receptor 4 (TLR4) and nuclear factor‐kappa B (NF‐κB) exhibited on oxidative stress in ALI. After the rats had been assigned into different groups, arterial blood, white blood cell (WBC), lung permeability index (LPI), wet/dry (W/D) ratio, TLR4 and NF‐κB expression and superoxide dismutase (SOD), myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) were examined. Afterward, the correlation between the levels of TLR4 and NF‐κB was determined. Decreased levels of PaO2, SOD, MPO, and GSH accompanied by increased levels of PaCO2, WBC number, LPI and W/D ratio, MDA and ROS, as well as TLR4 and NF‐κB expressions in the ALI, ALI + NF‐κB inhibitor, and ALI + phosphate buffer saline groups were found. Inhibition of NF‐κB resulted in increased PaO2 and decreased PaCO2 levels, WBC number, and LPI and W/D ratio. Decreased expression of NF‐κB increased SOD, GSH, and MPO, but decreased MDA and ROS. We also found that NF‐κB inhibition resulted in the improvement of ALI in rats. TLR4 and NF‐κB expressions were negatively correlated with levels of SOD, MPO, and GSH, and positively correlated with MDA and ROS levels. In summary, our findings provided evidence that inhibition of the TLR4/NF‐κB signaling pathway decreases oxidative stress, thereby improving ALI. As a result, NF‐κB signaling pathway has shown potential as a therapeutic target in ALI therapy.

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Section: Discussionsupporting

confidence: 69%

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Zhang

Wang

Chen

et al. 2019

The Kaohsiung J of Med Scie

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“…Kubota et al () reported dietary curcumin feeding significantly activated AMP‐activated kinase, decreased the expression of COX‐2 protein, and inhibited NF‐ κ B activity on the colonic mucosa of AOM‐ treated mice. In recent study investigation has shown that the anti‐metastatic effect of curcumin in CRC cell lines (LoVo and SW480) via AMPK activation and following inhibition of p65 NF‐κB, MMP9 and uPA (Tong, Wang, Sun, & Suo, ). Curcumin could significantly inhibited tumor growth and metastasis in mouse model of colorectal peritoneal carcinomatosis (CRPC).…”

Section: Discussionmentioning

confidence: 99%

Phytosomal curcumin inhibits tumor growth in colitis‐associated colorectal cancer

Marjaneh

Rahmani

Hassanian

et al. 2018

Journal Cellular Physiology

163

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Colorectal-cancer (CRC) is the third leading cause of death due to cancer, supporting the need for identification of novel anticancer drug to improve the efficacy of current-therapy. There is growing bodies of data showing the antitumor-activity of curcumin, although it is associated with low absorption. The aim of current study was explored the therapeutic-potential of novel phytosomal curcumin as well as its application in combination with 5-Flurouracil (5-FU) in a mouse-model of colitis-associated colon-cancer. The anti-proliferative-activity of phytosomal curcumin was assessed in 2- and 3-dimensional cell-culture-models as well as in a mouse-model of colitis-associated colon-cancer. The expression-levels of CyclinD1, beclin, E-cadherin, and p-GSK3a/b were investigated by qRT-PCR and/or Western-blotting. We evaluated the anti-inflammatory of this agent by pathological-evaluation and disease-activity-index (DAI). Moreover, oxidant/antioxidant activity was examined by malondialdehyde (MDA), total-thiols (T-SH), superoxide-dismutase (SOD), and catalase (CAT) activity parameters. Our data showed that phytosomal curcumin and its combination with 5-FU inhibited cell growth and invasive behavior of CRC cells through modulation of Wnt-pathway and E-cadherin. Combination of curcumin with 5-FU dramatically reduced the tumor-number and tumor-size in both distal and middle parts of colon in colitis-associated colon cancer followed by reduction in DAI. Also, curcumin suppressed the colonic inflammation and notably recovered the increased levels of MDA, decreased thiol level and reduced activity of CAT. We demonstrated the antitumor-activity of novel form of curcumin in CRC, supporting further investigations on the therapeutic-potential of this approach in colorectal-cancer.

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“…In addition, curcumin exerts an anti-inflammatory effect and protects cardiomyocytes against high glucose-induced apoptosis through this pathway (9,52). Additionally, previous studies demonstrated that the Wnt/β-catenin, Notch-1, nuclear factor-κB and mitogen-activated protein kinase signaling pathways were also involved in the effects of curcumin in cancer cells (51,(53)(54)(55)(56)(57), and these signaling pathways may also be involved in the growth-inhibitory effect of curcumin in LCSCs; however, this requires further investigation in future studies.…”

Section: Discussionmentioning

confidence: 99%

Curcumin inhibits the growth of liver cancer stem cells through the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway

Wang

2018

Exp Ther Med

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Abstract. Cancer stem cells are considered as a main cause of cancer recurrence. In the present study, the effects of curcumin on the growth of liver cancer stem cells (LCSCs) were investigated. The proliferation and apoptosis of LCSCs were assessed by MTT assays and flow cytometry. Changes in the expression of apoptosis-related proteins were identified by western blotting.The results of the study demonstrated that curcumin treatment inhibited the growth of LCSCs, induced cell apoptosis, as well as regulated the expression of apoptosis-associated proteins and the release of cytochrome c. Further experiments revealed that treatment with curcumin inhibited that the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Treatment with an activator of PI3K/AKT reversed the curcumin-induced growth inhibition of LCSCs. These results demonstrated that curcumin inhibited the growth of LCSCs through the PI3K/AKT/mTOR signaling pathway. Thus, the present study suggested that curcumin may be a potentially efficient agent in the treatment of liver cancer. IntroductionLiver cancer is one of the most common malignancies worldwide, with ~600,000 new cases diagnosed annually (1). However, the 5-year survival rate of liver cancer is <9% (2). This tumor is the fourth cause of cancer-associated mortality, ranking second in men and sixth in women, with >250,000 mortalities annually (1,3-5). At present, surgical resection is the major therapeutic strategy for liver cancer, although a high rate of recurrence remains (6,7).Stem cells are a type of cells harboring the ability to self-renew and differentiate (8). Cancer stem cells are a subset of cancer cells with stem cell properties. Although radiotherapy and chemotherapy can eliminate the majority of tumor cells, cancer stem cells have the ability to self-renew and differentiate to generate tumor cell heterogeneity, and thus resist these therapies (9). Liver cancer stem cells (LCSCs) are considered to account for the chemotherapy resistance and recurrence of liver cancer (10,11). Multiple signals pathways, including Notch and Wnt/β-catenin, are found to serve important roles in the stemness of LCSCs (12). The regulation of LCSCs via the manipulation of internal signaling pathways may become a feasible treatment for patients with liver cancer.Curcumin is a yellow natural compound derived from Rhizoma curcumae longae and is widely used as a spice in Asia. Curcumin has been demonstrated to exert anti-inflammatory, antioxidant and antiangiogenic effects (13-15), while it also exerts a potential antitumor effect (15-17). However, the effects of curcumin on LCSCs remain unclear. Therefore, the aim of the present study was to examine the effects of curcumin on the growth of LCSCs, as well as the underlying mechanism of its action. The study demonstrated that treatment with curcumin is able to inhibit the growth of LCSCs, and this compound may be a promising treatment agent for liver cancer. Materials and methodsC...

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Curcumin suppresses colon cancer cell invasion via AMPK-induced inhibition of NF–κB, uPA activator and MMP9

Cited by 114 publications

References 52 publications

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Phytosomal curcumin inhibits tumor growth in colitis‐associated colorectal cancer

Curcumin inhibits the growth of liver cancer stem cells through the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway

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