Clinical Cancer Research

2008

DOI: 10.1158/1078-0432.ccr-07-4722

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Curcumin Sensitizes Human Colorectal Cancer Xenografts in Nude Mice to γ-Radiation by Targeting Nuclear Factor-κB–Regulated Gene Products

Ajaikumar B. Kunnumakkara

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Parmeswaran Diagaradjane

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et al.

Abstract: Collectively, our results suggest that curcumin potentiates the antitumor effects of radiation therapy in colorectal cancer by suppressing NF-kappaB and NF-kappaB-regulated gene products, leading to inhibition of proliferation and angiogenesis.

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Cited by 199 publications

(145 citation statements)

References 58 publications

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“…This phytochemical also modulates various mechanisms that are associated with radioresistance, including the following: downregulating COX-2, MRP, Bcl-2, and survivin expression; inhibiting PI3K/AKT activation; suppressing growth factor signaling pathways; and inhibiting STAT3 activation (24)(25)(26). The present study demonstrated that Cur enhanced radiosensitivity in the NPC cell line CNE2 at 10 µmol/l by MTT or clonogenic survival test (27), although Cur exhibited higher anti-proliferative effects when used alone at a concentration of 20 or 40 µmol/l.…”

Section: Discussionmentioning

confidence: 99%

MiR-593 mediates curcumin-induced radiosensitization of nasopharyngeal carcinoma cells via MDR1

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et al. 2016

Oncology Letters

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Abstract. Curcumin (Cur) exhibits radiosensitization effects to a variety of malignant tumors. The present study investigates the radiosensitizing effect of Cur on nasopharyngeal carcinoma (NPC) cells and whether its mechanism is associated with microRNA-593 (miR-593) and multidrug resistance gene 1 (MDR1). A clonogenic assay was performed to measure the radiosensitizing effect. The expression of miR-593 and MDR1 was analyzed by quantitative polymerase chain reaction (qPCR) or western blot assay. A transplanted tumor model was established to identify the radiosensitizing effect in vivo. A luciferase-based reporter was constructed to evaluate the effect of direct binding of miR-593 to the putative target site on the 3' UTR of MDR1. The clonogenic assay showed that Cur enhanced the radiosensitivity of cells. Cur (100 mg/kg) combined with 4 Gy irradiation inhibited the growth of a transplanted tumor model in vivo, resulting in the higher inhibition ratio compared with the radiotherapy-alone group. These results demonstrated that Cur had a radiosensitizing effect on NPC cells in vivo and in vitro; Cur-mediated upregulation of miR-593 resulted in reduced MDR1 expression, which may promote radiosensitivity of NPC cells.

“…This phytochemical also modulates various mechanisms that are associated with radioresistance, including the following: downregulating COX-2, MRP, Bcl-2, and survivin expression; inhibiting PI3K/AKT activation; suppressing growth factor signaling pathways; and inhibiting STAT3 activation (24)(25)(26). The present study demonstrated that Cur enhanced radiosensitivity in the NPC cell line CNE2 at 10 µmol/l by MTT or clonogenic survival test (27), although Cur exhibited higher anti-proliferative effects when used alone at a concentration of 20 or 40 µmol/l.…”

Section: Discussionmentioning

confidence: 99%

MiR-593 mediates curcumin-induced radiosensitization of nasopharyngeal carcinoma cells via MDR1

¹

,

²

,

³

et al. 2016

Oncology Letters

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Abstract. Curcumin (Cur) exhibits radiosensitization effects to a variety of malignant tumors. The present study investigates the radiosensitizing effect of Cur on nasopharyngeal carcinoma (NPC) cells and whether its mechanism is associated with microRNA-593 (miR-593) and multidrug resistance gene 1 (MDR1). A clonogenic assay was performed to measure the radiosensitizing effect. The expression of miR-593 and MDR1 was analyzed by quantitative polymerase chain reaction (qPCR) or western blot assay. A transplanted tumor model was established to identify the radiosensitizing effect in vivo. A luciferase-based reporter was constructed to evaluate the effect of direct binding of miR-593 to the putative target site on the 3' UTR of MDR1. The clonogenic assay showed that Cur enhanced the radiosensitivity of cells. Cur (100 mg/kg) combined with 4 Gy irradiation inhibited the growth of a transplanted tumor model in vivo, resulting in the higher inhibition ratio compared with the radiotherapy-alone group. These results demonstrated that Cur had a radiosensitizing effect on NPC cells in vivo and in vitro; Cur-mediated upregulation of miR-593 resulted in reduced MDR1 expression, which may promote radiosensitivity of NPC cells.

“…Bimonte et al [175] reported that curcumin inhibits the expression of MMP-9 in orthotopically implanted pancreatic tumors. Curcumin causes a significant reduction of tumor volume, and MMP-9 activity in a xenografted model [176] . Curcumin also reduces the expression of major MMPs via reduced NFκB activity and AP-1 transcription [176] .…”

Section: Curcuminmentioning

confidence: 93%

“…Curcumin causes a significant reduction of tumor volume, and MMP-9 activity in a xenografted model [176] . Curcumin also reduces the expression of major MMPs via reduced NFκB activity and AP-1 transcription [176] . Lin et al [177] reported that curcumin inhibits SK-Hep-1 hepatocellular carcinoma cell invasion via suppression of MMP-9 secretion.…”

Section: Curcuminmentioning

confidence: 93%

Matrix metalloproteinases and gastrointestinal cancers: Impacts of dietary antioxidants

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et al. 2014

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teinase (TIMP) which bind MMPs with a 1:1 stoichiometry. In addition, RECK (reversion including cysteinerich protein with kazal motifs) is a membrane bound glycoprotein that inhibits MMP-2, -9 and -14. Moreover, α2-macroglobulin mediates the uptake of several MMPs thereby inhibit their activity. Cancerous conditions increase intrinsic reactive oxygen species (ROS) through mitochondrial dysfunction leading to altered protease/ anti-protease balance. ROS, an index of oxidative stress is also involved in tumorigenesis by activation of different MAP kinase pathways including MMP induction. Oxidative stress is involved in cancer by changing the activity and expression of regulatory proteins especially MMPs. Epidemiological studies have shown that high intake of fruits that rich in antioxidants is associated with a lower cancer incidence. Evidence indicates that some antioxidants inhibit the growth of malignant cells by inducing apoptosis and inhibiting the activity of MMPs. This review is discussed in six subchapters, as follows. AbstractThe process of carcinogenesis is tightly regulated by antioxidant enzymes and matrix degrading enzymes, namely, matrix metalloproteinases (MMPs). Degradation of extracellular matrix (ECM) proteins like collagen, proteoglycan, laminin, elastin and fibronectin is considered to be the prerequisite for tumor invasion and metastasis. MMPs can degrade essentially all of the ECM components and, most MMPs also substantially contribute to angiogenesis, differentiation, proliferation and apoptosis. Hence, MMPs are important regulators of tumor growth both at the primary site and in distant metastases; thus the enzymes are considered as important targets for cancer therapy. The implications of MMPs in cancers are no longer mysterious; however, the mechanism of action is yet to be explained. Herein, our major interest is to clarify how MMPs are tied up with gastrointestinal cancers. Gastrointestinal cancer is a variety of cancer types, including the cancers of gastrointestinal tract and organs, i.e., esophagus, stomach, biliary system, pancreas, small intestine, large intestine, rectum and anus. The activity of MMPs is regulated by its endogenous inhibitor tissue inhibitor of metallopro-

“…Classified as type I programed cell death, apoptosis is involved in a number of cancer-related processes, including tumorigenesis, tumor progression and cellular responses to chemotherapy and radiotherapy (4)(5)(6). The well-studied tumor suppressor protein, p53, is key to apoptosis and cancer development.…”

Section: Introductionmentioning

confidence: 99%

High p53 and MAP1 light chain 3A co-expression predicts poor prognosis in patients with esophageal squamous cell carcinoma

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et al. 2013

Molecular Medicine Reports

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Abstract. p53 and microtubule-associated protein 1 light chain 3A (LC3A) are regulators of apoptosis and autophagy and are expressed at high levels in a number of human tumors. The purpose of the current study was to evaluate the clinicopathological and prognostic significance of p53 and LC3A expression levels in esophageal squamous cell carcinomas (ESCCs). p53 and LC3A expression levels were measured by immunohistochemistry in 114 patients with stage II/III (T any N+M 0 or T 3,4 N any M 0 ) ESCCs treated with surgery followed by adjuvant concurrent chemoradiotherapy. The overexpression of p53 and LC3A was observed in 57 and 54% of ESCC samples, respectively. p53 staining was nuclear and LC3A was localized to the cytoplasm of tumor cells. p53 overexpression was more frequently observed in ESCCs with positive lymph nodes (P=0.017). Patients with ESCCs overexpressing p53 and LC3A were associated with a lower 5-year overall survival rate than those with low p53 and LC3A expression (18.0 vs. 54.4%; P=0.001). Univariate and multivariate analyses revealed that the overexpression of p53 or LC3A was not associated with poor patient outcome (P>0.05). However, patients with high levels of p53 and LC3A co-expression had poor clinical prognoses (P=0.027). Thus, p53 and LC3A co-expression is an independent prognostic marker for patients with ESCC. IntroductionEsophageal carcinoma (EC) is a public health issue in China (1). It has a poor overall prognosis and treatment outcomes for patients with EC have not improved over the last few decades. Significant prognostic indicators include the extent of invasion and lymph node and distal metastases (2). However, specific patients with the same stage have different prognosis (3). Therefore, molecular markers to improve the outcome prediction for patients with EC must be identified.Classified as type I programed cell death, apoptosis is involved in a number of cancer-related processes, including tumorigenesis, tumor progression and cellular responses to chemotherapy and radiotherapy (4-6). The well-studied tumor suppressor protein, p53, is key to apoptosis and cancer development. Wild-type p53 inhibits tumor growth by inducing apoptosis and inhibiting angiogenesis and metastasis; however, the TP53 gene undergoes inactivating mutations in a variety of cancer types. More recently, p53 has been demonstrated to repress autophagy (7), indicating that apoptosis and autophagy may interact. Type II programmed cell death, or autophagy, is an evolutionarily conserved eukaryotic process important for maintaining homeostasis by recycling stable proteins and long-lived organelles (8).Autophagy is important in a number of physiological processes, including adaptation to hypoxia, prevention of tumorigenesis and antigen presentation (9-11). Although the role of autophagy in cancer is unclear, the current view is that it functions as a cytoprotective mechanism during tumor progression (12).Previously, microtubule-associated protein 1 light chain 3A (LC3A), one of three microtubule-associated protein ...

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