Synergistic Effect of Curcumin in Combination with Anticancer Agents in Human Retinoblastoma Cancer Cell Lines

Sreenivasan, Seethalakshmi; Krishnakumar, Subramanian

doi:10.3109/02713683.2014.987870

Cited by 31 publications

(10 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recently, several researchers also focused on the potential role of curcumin in Rb. Sreenivasan and his colleagues have reported that curcumin suppressed the expression of multidrug resistance associated protein 1 (MDR1) [ 29 ], thereby rendering Rb cells more sensitive to chemotherapy [ 30 ]. Another investigation demonstrated that curcumin induced the apoptosis of Y79 cells possibly through activating JNK and p38 MAPK pathways [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Curcumin inhibits proliferation, migration, invasion and promotes apoptosis of retinoblastoma cell lines through modulation of miR-99a and JAK/STAT pathway

Sun

Han

et al. 2018

BMC Cancer

View full text Add to dashboard Cite

BackgroundCurcumin, a primary active ingredient extracted from the Curcuma longa, has been recently identified as a potential anti-tumor agent in multiple kinds of cancers. However, the effect of curcumin on retinoblastoma (Rb) is still unclear. Therefore, we attempted to reveal the functional impacts and the underlying mechanisms of curcumin in Rb cells.MethodsTwo Rb cell lines SO-Rb50 and Y79 were pre-treated with various doses of curcumin, and then cell proliferation, apoptosis, migration, and invasion were assessed, respectively. Further, regulatory effects of curcumin on miR-99a expression, as well as the activation of JAK/STAT pathway were studied.ResultsData showed that curcumin significantly inhibited the viability, colony formation capacity, migration and invasion, while induced apoptosis of SO-Rb50 and Y79 cells. Up-regulation of miR-99a was observed in curcumin-treated cells. Curcumin suppressed the phosphorylation levels of JAK1, STAT1, and STAT3, while curcumin did not inhibit the activation of JAK/STAT pathway when miR-99a was knocked down.ConclusionCurcumin inhibited proliferation, migration, invasion, but promoted apoptosis of Rb cells. The anti-tumor activities of curcumin on Rb cells appeared to be via up-regulation of miR-99a, and thereby inhibition of JAK/STAT pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Curcumin inhibits proliferation, migration, invasion and promotes apoptosis of retinoblastoma cell lines through modulation of miR-99a and JAK/STAT pathway

Sun

Han

et al. 2018

BMC Cancer

View full text Add to dashboard Cite

show abstract

“… 34 Intensifying the effect of curcumin on the cytotoxic action of etoposide has been demonstrated in brain tumor and retinoblastoma cell lines. 35 , 36 In the present study, curcumin potentiated the cytotoxic effect of etoposide in HL-60 cells through intensification of its genotoxicity, which is indicated by the significant increase in the amount of γ-H2AX after treatment with a combination of curcumin and etoposide, accompanied by a corresponding increase in the percentage of the sub-G1 fraction in comparison to the cytostatic drug alone.…”

Section: Discussionsupporting

confidence: 57%

Curcumin enhances the cytogenotoxic effect of etoposide in leukemia cells through induction of reactive oxygen species

Papież¹,

Krzyściak²,

Szade³

et al. 2016

DDDT

View full text Add to dashboard Cite

Curcumin may exert a more selective cytotoxic effect in tumor cells with elevated levels of free radicals. Here, we investigated whether curcumin can modulate etoposide action in myeloid leukemia cells and in normal cells of hematopoietic origin. HL-60 cell line, normal myeloid progenitor cluster of differentiation (CD)-34+ cells, and granulocytes were incubated for 4 or 24 hours at different concentrations of curcumin and/or etoposide. Brown Norway rats with acute myeloid leukemia (BNML) were used to prove the influence of curcumin on etoposide action in vivo. Rats were treated with curcumin for 23 days and etoposide was administered for the final 3 days of the experiment. Curcumin synergistically potentiated the cytotoxic effect of etoposide, and it intensified apoptosis and phosphorylation of the histone H2AX induced by this cytostatic drug in leukemic HL-60 cells. In contrast, curcumin did not significantly modify etoposide-induced cytotoxicity and H2AX phosphorylation in normal CD34+ cells and granulocytes. Curcumin modified the cytotoxic action of etoposide in HL-60 cells through intensification of free radical production because preincubation with N-acetyl-l-cysteine (NAC) significantly reduced the cytotoxic effect of curcumin itself and a combination of two compounds. In contrast, NAC did not decrease the cytotoxic effect of etoposide. Thus, oxidative stress plays a greater role in the cytotoxic effect of curcumin than that of etoposide in HL-60 cells. In vitro results were confirmed in a BNML model. Pretreatment with curcumin enhanced the antileukemic activity of etoposide in BNML rats (1.57-fold tumor reduction versus etoposide alone; P<0.05) and induced apoptosis of BNML cells more efficiently than etoposide alone (1.54-fold change versus etoposide alone; P<0.05), but this treatment protected nonleukemic B-cells from apoptosis. Thus, curcumin can increase the antileukemic effect of etoposide through reactive oxygen species in sensitive myeloid leukemia cells, and it is harmless to normal human cells.

show abstract

“…In a previous study, ATG exhibited increased antitumor activity against retinoblastoma cells compared with carboplatin in vitro (18,19), indicating its potential clinical value in the treatment of retinoblastoma; however, ATG does not represent a current available therapy to treat patients with retinoblastoma, to the best of our knowledge. The antitumor potential of ATG has been demonstrated in various types of cancer in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 90%

The antitumor function of arctigenin in human retinoblastoma cells is mediated by jagged‑1

Ning

Liu

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

Retinoblastoma is an intraocular malignant tumor that may severely affect vision and represents a life-threatening disease in children. Arctigenin (ATG) is an active compound that exhibits numerous pharmacological activities, which is isolated from the seeds of greater burdock ( Arctium lappa Linnaeus), a plant used in traditional Chinese herbal medicine. The present study aimed to investigate the effects of ATG on cancer progression by analyzing the retinoblastoma cell line Y79. ATG exhibited a significant inhibitory effect on the viability of Y79 cells in a dose-dependent manner. Furthermore, treatment with ATG promoted apoptosis, and increased the protein expression levels of B-cell lymphoma 2 (BCL-2)-associated X protein and decreased the protein expression levels of BCL-2. Cell migration was suppressed following treatment with ATG, as assessed by Transwell migration assay. Furthermore, the protein expression levels of jagged-1 (JAG1) were decreased, and various factors involved in the Notch signaling pathway, including the Notch intracellular domain (NICD), transcription factor HES (HES)5 and HES1 were downregulated following treatment with ATG. The decreased expression levels of JAG1 were restored in response to JAG1 overexpression, alongside increases in the protein expression levels of NICD, HES5 and HES1. Furthermore, overexpression of JAG1 partly restored the cell viability and migration suppressed following treatment with ATG. In addition, ATG-induced apoptosis was reduced by JAG1 overexpression. Collectively, the present results suggested that ATG may serve as an antitumor compound by suppressing the proliferation and migration of retinoblastoma cells, inducing apoptosis, downregulating the protein expression levels of JAG1, and decreasing the activity of the Notch signaling pathway.

show abstract

Synergistic Effect of Curcumin in Combination with Anticancer Agents in Human Retinoblastoma Cancer Cell Lines

Cited by 31 publications

References 30 publications

RETRACTED ARTICLE: Curcumin inhibits proliferation, migration, invasion and promotes apoptosis of retinoblastoma cell lines through modulation of miR-99a and JAK/STAT pathway

RETRACTED ARTICLE: Curcumin inhibits proliferation, migration, invasion and promotes apoptosis of retinoblastoma cell lines through modulation of miR-99a and JAK/STAT pathway

Curcumin enhances the cytogenotoxic effect of etoposide in leukemia cells through induction of reactive oxygen species

The antitumor function of arctigenin in human retinoblastoma cells is mediated by jagged‑1

Contact Info

Product

Resources

About