Curcumin Enhances the Radiosensitivity of U87 Cells by Inducing DUSP-2 Up-Regulation

Qian, Yu; José, Ma; Guo, Xiaoyi; Sun, Jun; Yu, Yangyang; Cao, Boqiang; Zhang, Lei; Ding, Xiaopeng; Jin, Hui‐Zi; Shao, Jian‐Fu

doi:10.1159/000373959

Cited by 41 publications

(24 citation statements)

References 25 publications

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“…Glioblastoma multiforme (GBM) is the most aggressive brain tumour in humans and is regulated by many different molecules [26,27]. The microenvironment of glioblastomas seems to be restricted when the expression of KIF14 is inhibited [28] or due to low doses given of curcumin [29]. Furthermore, the tumour growth and progression of gliomas has been shown to be diminished in case of inhibition of autophagy in late stages [30].…”

Section: Introductionmentioning

confidence: 99%

The Role of RhoA, RhoB and RhoC GTPases in Cell Morphology, Proliferation and Migration in Human Cytomegalovirus (HCMV) Infected Glioblastoma Cells

Tseliou

Al‐Qahtani²,

Alarifi

et al. 2016

Cell Physiol Biochem

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Background/Aims: Rho GTPases are crucial regulators of the actin cytoskeleton, membrane trafficking and cell signaling and their importance in cell migration and invasion is well- established. The human cytomegalovirus (HCMV) is a widespread pathogen responsible for generally asymptomatic and persistent infections in healthy people. Recent evidence indicates that HCMV gene products are expressed in over 90% of malignant type glioblastomas (GBM). In addition, the HCMV Immediate Early-1 protein (IE1) is expressed in >90% of tumors analyzed. Methods: RhoA, RhoB and RhoC were individually depleted in U373MG glioblastoma cells as well as U373MG cells stably expressing the HCMV IE1 protein (named U373MG-IE1 cells) shRNA lentivirus vectors. Cell proliferation assays, migration as well as wound-healing assays were performed in uninfected and HCMV-infected cells. Results: The depletion of RhoA, RhoB and RhoC protein resulted in significant alterations in the morphology of the uninfected cells, which were further enhanced by the cytopathic effect caused by HCMV. Furthermore, in the absence or presence of HCMV, the knockdown of RhoB and RhoC proteins decreased the proliferation rate of the parental and the IE1-expressing glioblastoma cells, whereas the knockdown of RhoA protein in the HCMV infected cell lines restored their proliferation rate. In addition, wound healing assays in U373MG cells revealed that depletion of RhoA, RhoB and RhoC differentially reduced their migration rate, even in the presence or the absence of HCMV. Conclusion: Collectively, these data show for the first time a differential implication of Rho GTPases in morphology, proliferation rate and motility of human glioblastoma cells during HCMV infection, further supporting an oncomodulatory role of HCMV depending on the Rho isoforms' state.

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Section: Introductionmentioning

confidence: 99%

The Role of RhoA, RhoB and RhoC GTPases in Cell Morphology, Proliferation and Migration in Human Cytomegalovirus (HCMV) Infected Glioblastoma Cells

Tseliou

Al‐Qahtani²,

Alarifi

et al. 2016

Cell Physiol Biochem

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“…Presently, investigations have been performed on the effects of many radio-sensitizing reagents, including Curricumin [11], Celecoxib [12], and Saikosaporin [13], and specific inhibitors, such as YM155 [14] (inhibitor of survinin) and DNA-PK inhibitors. NU7441, a derivative from LY294002, is a synthetic and specific DNA-PK inhibitor.…”

Section: Introductionmentioning

confidence: 99%

NU7441 Enhances the Radiosensitivity of Liver Cancer Cells

Yang

Wang

Liu

et al. 2016

Cell Physiol Biochem

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Objective: Radiation therapy, one of the major treatments for liver cancer, causes DNA damage and cell death. Since the liver cancer cells have a strong capacity to repair irradiative injury, new medicines to enhance this treatment are urgently required. In this study, we investigated the effect of NU7441, a synthetic small-molecule compound, as a specific inhibitor of DNA-dependent protein kinase (DNA-PK) in radiosensitization of hepatocellular carcinoma HepG2 cells. Methods: Cell Counting Kit-8 (CCK-8) was first used to evaluate the proliferation of HepG2 cells under NU7441 treatment. SDS-PAGE and Western blot were then performed to study the protein expression leading to the DNA damage repair. Further, neutral single cell gel electrophoresis and immunofluorescence assay were carried out to assess DNA repair. Finally, flow cytometry was implemented to examine the changes in cell cycle. Results: NU7441 reduced the CCK-8 counts in the HepG2 culture, further enhanced ⁶⁰Coγ radiation injury to HepG2 cells, which was manifested by decreasing the DNA-PKcs (S2056) protein expression, increasing γH2AX foci number, prolonging the tail moment of the comet cells, and inducing cell cycle arrest at G2/M phase. Conclusion: NU7441 inhibited the growth of liver cancer cells, enhanced the radiosensitization of these cancer cells by interfering with the DNA repair and cell cycle checkpoint. These data implicate NU7441 as a potential radiotherapy sensitizer for the treatment of liver cancer.

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“…Curcumin, which is termed as 1,7-bis(4-hydroxy-3-m e t h o x y p h e n y l ) -1 , 6 -h e p a t a d i e n e -3 , 5 -d i o n e , o r diferulolylmethane, is a major constituent of the yellow spice turmeric that is extracted from the rhizome of the plant Curcuma longa [9][10][11][12][13]. Curcumin has been shown of anticancer effects in a number of cancers, including PC [9,[14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

“…Curcumin has been shown of anticancer effects in a number of cancers, including PC [9,[14][15][16][17][18]. Although the previous studies have shown that Curcumin induces significant cancer cell death at high dose [14][15][16][17][18], there are so far no studies on the effects of low-dose Curcumin on cancer cells, which may be more clinically applicable due to lack of various side effects due to use of high dose of Curcumin.…”

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits growth of prostate carcinoma via miR-208-mediated CDKN1A activation

Guo

Yang

2015

Tumor Biol.

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Prostate cancer (PC) is a prevalent cancer in aged men. Curcumin is an active ingredient that has been extracted from the rhizome of the plant Curcuma longa. Recently, a potential of Curcumin against PC has been reported in PC, whereas the underlying molecular mechanisms are not completely understood. Here, we studied the effects of low-dose Curcumin on PC cell growth. Curcumin (from 0.2 to 0.8 μmol/l) dose-dependently inhibited the proliferation of PC cells, without affecting cell apoptosis. Further analyses showed that Curcumin dose-dependently increased a cell cycle suppressor CDKN1A at protein levels, but not mRNA levels, in PC cells, suggesting that Curcumin may regulate the translation of CDKN1A, as well as a possible involvement of miRNA intervention. From all CDKN1A-3'-UTR-binding miRNAs, we found that miR-208 was specifically inhibited in PC cells dose-dependently by Curcumin. Moreover, miR-208 was found to bind CDKN1A to suppress its expression. In a loss-of-function experiment, PC cells that overexpressed miR-208 failed to decrease cell proliferation in response to Curcumin. Together, these data suggest that Curcumin inhibits growth of PC via miR-208-mediated CDKN1A activation.

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Curcumin Enhances the Radiosensitivity of U87 Cells by Inducing DUSP-2 Up-Regulation

Cited by 41 publications

References 25 publications

The Role of RhoA, RhoB and RhoC GTPases in Cell Morphology, Proliferation and Migration in Human Cytomegalovirus (HCMV) Infected Glioblastoma Cells

The Role of RhoA, RhoB and RhoC GTPases in Cell Morphology, Proliferation and Migration in Human Cytomegalovirus (HCMV) Infected Glioblastoma Cells

NU7441 Enhances the Radiosensitivity of Liver Cancer Cells

Curcumin inhibits growth of prostate carcinoma via miR-208-mediated CDKN1A activation

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