Curcumin Conjugates Induce Apoptosis Via a Mitochondrion Dependent Pathway in MCF-7 and MDA-MB-231 Cell Lines

Singh, Durg Vijay; Agarwal, Shikha; Singh, Preeti; Godbole, Madan M.; Misra, Krishna

doi:10.7314/apjcp.2013.14.10.5797

Cited by 28 publications

(16 citation statements)

References 52 publications

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“…The combination of curcumin and MMC significantly reduce the MDA-MB-231 and MCF-7. It has been reported that curcumin induced apoptosis in MDA-MB-231 cells through other pathways [ 39 – 41 ]. Moreover, MDA-MB-231 cells are more metastatic than MCF-7.…”

Section: Discussionmentioning

confidence: 99%

Curcumin reduces mitomycin C resistance in breast cancer stem cells by regulating Bcl-2 family-mediated apoptosis

Zhou

Sun

et al. 2017

Cancer Cell Int

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BackgroundCurcumin, a natural compound derived from the turmeric rhizome Curcuma longa Linn, has anticancer and chemoresistance reduction biological activities. We evaluated the efficacy of curcumin in sensitizing chemotherapy drugs through regulation of Bcl-2-mediated apoptosis in breast cancer stem-like cells (BCSCs).MethodsCell survival was measured using MTT assay. Apoptosis-related proteins were observed using western blot analysis. Apoptosis was detected with flow cytometric analysis and by Hoechst 33258 staining. The mitochondrial membrane potential was observed with flow cytometric analysis.ResultsThe ability of BCSCs to propagate decreased gradually along the passages and was completely lost at the fifth passage [0.1 μmol/L mitomycin C (MMC) with 5 μmol/L curcumin in MCF-7 and 0.5 μmol/L MMC with 5 μmol/L curcumin in MDA-MB-231 cells]. Curcumin combined with MMC treatment significantly decreased the levels of antiapoptotic Bcl-2 and Bcl-w expression, increased the levels of proapoptotic Bax, Bak, Bad, Bik, and Bim expression, and activated caspase-3 and caspase-9 in MCF-7 BCSCs. In the presence of Bcl-2 siRNA, the apoptosis rate increased by 15% in cells treated with curcumin and MMC. The mitochondrial membrane potential decreased by approximately 20% in MCF-7 BCSCs undergoing the combination treatment of curcumin and MMC. The combination-induced decrease in Bcl-2 was regulated by the presence of the Wnt-specific inhibitor PFK115-584 and PI3k inhibitor LY294002.ConclusionsOur study indicates that curcumin might represent a novel therapeutic agent for treating breast cancer chemoresistance induced by MMC.

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Section: Discussionmentioning

confidence: 99%

Curcumin reduces mitomycin C resistance in breast cancer stem cells by regulating Bcl-2 family-mediated apoptosis

Zhou

Sun

et al. 2017

Cancer Cell Int

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“…Apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies (Wong, 2011;Li et al, 2013;Singh et al, 2013;Gopal et al, 2014;. The abundance of literature suggests that targeting apoptosis in cancer is feasible.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Induces Apoptosis in SGC-7901 Gastric Adenocarcinoma Cells via Regulation of Mitochondrial Signaling Pathways

Xue¹,

Yu²,

Sun³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Curcumin, a polyphenol compound derived from the rhizome of the plant Curcuma longa L. has been verified as an anticancer compound against several types of cancer. However, understanding of the molecular mechanisms by which it induces apoptosis is limited. In this study, the anticancer efficacy of curcumin was investigated in human gastric adenocarcinoma SGC-7901 cells. The results demonstrated that curcumin induced morphological changes and decreased cell viability. Apoptosis triggered by curcumin was visualized using Annexin V-FITC/7-AAD staining. Curcumin-induced apoptosis of SGC-7901 cells was associated with the dissipation of mitochondrial membrane potential (MMP) and the release of cytochrome c into the cytosol. Furthermore, the down-regulation of Bcl-2 and up-regulation of Bax that led to the cleavage of caspase-3 and increased cleaved PARP was observed in SGC-7901 cells treated with curcumin. Therefore, curcumin-induced apoptosis of SGC-7901 cells might be mediated through the mitochondria pathway, which gives the rationale for in vivo studies on the utilization of curcumin as a potential cancer therapeutic compound.

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“…9 ), which confirmed the involvement of mitochondrial pathway. Bax and Bak translocate from cytoplasm to mitochondrial outer membrane forming channel for protein release from mitochondrial intermembranous space, such as cytochrome c, Smac/Diablo, and apoptosis inducing factor (AIF) [ 32 ] to mediate apoptosis characters, which are formation of apoptosome, DNA degradation, and activation of caspase-9 and 3. Caspase-8-activated proteolysis of Bid can be mediated from the death receptor to mitochondrial dysfunction pathway as demonstrated by an increase in truncated Bid (tBid) level (Fig.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin from Citrus seed induces human hepatocellular carcinoma HepG2 cell apoptosis via both mitochondrial and death receptor pathways

et al. 2015

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Citrus seeds are full of phenolic compounds, such as flavonoids. The aims of this study were to identify the types of flavonoids in Citrus seed extracts, the cytotoxic effect, mode of cell death, and signaling pathway in human hepatic cancer HepG2 cells. The flavonoids contain anticancer, free radical scavenging, and antioxidant activities. Neohesperidin, hesperidin, and naringin, active flavanone glycosides, were identified in Citrus seed extract. The cytotoxic effect of three compounds was in a dose-dependent manner, and IC50 levels were determined. The sensitivity of human HepG2 cells was as follows: hesperidin > naringin > neohesperidin > naringenin. Hesperidin induced HepG2 cells to undergo apoptosis in a dose-dependent manner as evidenced by the externalization of phosphatidylserine and determined by annexin V-fluorescein isothiocyanate and propidium iodide staining using flow cytometry. Hesperidin did not induce the generation of reactive oxygen species, which was determined by using 2′,7′-dichlorohydrofluorescein diacetate and flow cytometry method. The number of hesperidin-treated HepG2 cells with the loss of mitochondrial transmembrane potential increased concentration dependently, using 3,3′-dihexyloxacarbocyanine iodide employing flow cytometry. Caspase-9, -8, and -3 activities were activated and increased in hesperidin-treated HepG2 cells. Bcl-xL protein was downregulated whereas Bax, Bak, and tBid protein levels were upregulated after treatment with hesperidin in a dose-dependent manner. In conclusion, the bioflavanone from Citrus seeds, hesperidin, induced human HepG2 cell apoptosis via mitochondrial pathway and death receptor pathway. Citrus seed flavonoids are beneficial and can be developed as anticancer drug or food supplement, which still needs further in vivo investigation in animals and human beings.

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Curcumin Conjugates Induce Apoptosis Via a Mitochondrion Dependent Pathway in MCF-7 and MDA-MB-231 Cell Lines

Cited by 28 publications

References 52 publications

Curcumin reduces mitomycin C resistance in breast cancer stem cells by regulating Bcl-2 family-mediated apoptosis

Curcumin reduces mitomycin C resistance in breast cancer stem cells by regulating Bcl-2 family-mediated apoptosis

Curcumin Induces Apoptosis in SGC-7901 Gastric Adenocarcinoma Cells via Regulation of Mitochondrial Signaling Pathways

Hesperidin from Citrus seed induces human hepatocellular carcinoma HepG2 cell apoptosis via both mitochondrial and death receptor pathways

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