Curcumin modulates cellular AP-1, NF-kB, and HPV16 E6 proteins in oral cancer

Mishra, Alok; Kumar, Rakesh; Tyagi, Abhishek; Kohaar, Indu; Hedau, Suresh; Bharti, Alok C.; Sarker, Subhodeep; Dey, Dipankar; Saluja, Daman; Das, Bhudev C.

doi:10.3332/ecancer.2015.525

Cited by 66 publications

(61 citation statements)

References 33 publications

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“…However, NF-kB affords tumor cell protection by inducing Bcl-2 expression, whereas p53 promotes apoptosis by boosting the expression of the pro-apoptotic protein Bax [ 21 ]. Curcumin causes inactivation of the transcription factors AP-1 and NF-kB, which have been implicated in the transcription of HPV-associated proteins such as E6 and E7 [ 22 ]. This curcumin-evoked inhibition of NF-kB and the consequent suppression of E6 [ 21 ], leads to induction of p53, suppression of the NF-kB-Bcl-2 protective pathway, and preferential stimulation of the p53-Bax apoptotic pathway in cancer cells [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Unique synergistic formulation of curcumin, epicatechin gallate and resveratrol, tricurin, suppresses HPV E6, eliminates HPV+ cancer cells, and inhibits tumor progression

et al. 2017

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Curcumin (from curry) (C) is highly potent against cervical cancer cells (CCC), but poor bioavailability has limited its clinical use. Similar natural polyphenols resveratrol (from grapes) (R), and epicatechin gallate (from green tea) (E) also display activity against CCC. By treating CCC (HeLa) with C, E, or R, or combinations of these compounds, we computed combination indices and observed a strong synergism among C, E, and R at the unique molar ratio 4:1:12.5. This combination, named as TriCurin, rapidly down regulated HPV18 E6 and NF-kB expression while concomitantly inducing the tumor suppressor protein p53 in HeLa cells. In the mouse c-Ha-ras and HPV16 E6, E7-expressing TC-1 CCC, both C and TriCurin elicited suppression of E6, induction of both p53 and acetyl-p53 (activated p53), and activation of caspase-3, but the TriCurin-evoked changes were several-fold greater than that produced by curcumin (4.7-fold for E6 inhibition, and 2-fold, 6-fold, and 1.7-fold for the induction of p53, acetyl-p53, and active caspase-3, respectively). Consequently, TriCurin was more potent in killing TC-1 and HeLa cells. Intralesional TriCurin treatment of tumors generated in mice by subcutaneously implanting the TC-1 CCC caused an 80–90% decrease in tumor growth. The ability of C to eliminate HeLa cells was significantly stabilized when delivered as TriCurin than when delivered alone. Topical application of TriCurin dispersed in a cream base afforded efficient transfer of C across the skin. Subcutaneous TriCurin injection yielded no adverse effect in tumor-naïve healthy mice. Thus, TriCurin is a safe and promising therapeutic agent against HPV-associated disease.

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Section: Discussionmentioning

confidence: 99%

Unique synergistic formulation of curcumin, epicatechin gallate and resveratrol, tricurin, suppresses HPV E6, eliminates HPV+ cancer cells, and inhibits tumor progression

et al. 2017

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“…Curcumin, a pharmacologically safe herbal compound is known for its anticancer effects, including inhibition of proliferation and angiogenesis, induction of apoptosis and increased chemo-radiosensitivity ( 8 – 11 ).Recent studies have demonstrated curcumin as a potent inhibitor of AP-1, NF-kB, and HPV in cervical and oral cancer ( 11 – 15 ) but its effects on oral cancer and CSCs with or without HPV infection are unknown. Therefore, the present study was performed to clarify the effects of curcumin in OSCC-CSCs.…”

Section: Introductionmentioning

confidence: 99%

Differential Inhibitory Effects of Curcumin Between HPV+ve and HPV–ve Oral Cancer Stem Cells

2018

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Aim: To investigate the role of a herbal antioxidative compound curcumin on cell proliferation, orosphere formation and miRNA-21 expression in HPV16+ve/–ve oral cancer stem cells.Materials and Methods: Oral cancer stem cells were isolated from HPV+ve/HPV–ve oral cancer cell lines by FACS and stemness markers. MTT, spheroid assay and qRT-PCR were employed to examine the effects of curcumin.Results: Curcumin treatment in micromolar concentration (0–50 μM) demonstrated significant differential inhibition in CSC proliferation, orosphere formation and miRNA-21 expression in a dose dependent manner, the effect being highly pronounced in HPV positive CSCs.Conclusion: The strong and dose-dependent inhibitory effects of curcumin on cell proliferation, stemness and miRNA appear to be due to its chemosensitizing and anticancer effects on OSCC-CSCs.

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“…As a natural compound, it has been proven to be effective with minimal toxicity, which selectively acts on cancer cells over normal cells (5,6). Hitherto, curcumin and its analog have been reported to play an anticancer role in several tumor models, including glioblastoma (7), liver (8), colorectal (9), lung (10), ovarian (11), breast (12) and oral (13) cancer. The underlying mechanisms have been demonstrated to be associated with the inhibition of proliferation, angiogenesis, invasion and metastasis of cancer cells, or apoptosis induction by curcumin (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

Zhou

Yang

et al. 2017

Oncology Reports

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Abstract. Curcumin possesses an anticancer effect against a wide assortment of tumors with selective cytotoxicity for tumor cells. However, the mechanism involved in the curcumin-induced anticancer effect remain unclear. In the present study, we investigated the efficacy of curcumin against human gastric cancer cell growth and the molecular mechanism involved. Our results demonstrated that curcumin inhibited the viabilities of gastric cancer cell lines BGC-823, SGC-7901 and MKN-28 in both a time-and dose-dependent manner. In addition, curcumin treatment induced gastric cancer cell apoptosis in a dose-responsive manner. Western blotting of apoptosis-related proteins further confirmed the pro-apoptotic potential of curcumin. After exposure to curcumin, a robust induction of autophagy was observed in gastric cancer cells, which was characterized by the formation of acidic vesicular organelles (AVOs), conversion of LC3-I to LC3-II and an increase in the levels of autophagy-related proteins. Activation of the PI3K/Akt/mTOR signaling pathway was suppressed in gastric cancer cells with curcumin treatment. However, administration of the autophagy inhibitor 3-methyladenine (3-MA) significantly promoted the apoptotic cell death induced by curcumin. Collectively, our findings provide new evidence that curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells in vitro. Autophagy inhibitor treatment may provide a novel and effective strategy for improving the anticancer effect of curcumin against gastric cancer.

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Curcumin modulates cellular AP-1, NF-kB, and HPV16 E6 proteins in oral cancer

Cited by 66 publications

References 33 publications

Unique synergistic formulation of curcumin, epicatechin gallate and resveratrol, tricurin, suppresses HPV E6, eliminates HPV+ cancer cells, and inhibits tumor progression

Unique synergistic formulation of curcumin, epicatechin gallate and resveratrol, tricurin, suppresses HPV E6, eliminates HPV+ cancer cells, and inhibits tumor progression

Differential Inhibitory Effects of Curcumin Between HPV+ve and HPV–ve Oral Cancer Stem Cells

Curcumin induces apoptotic cell death and protective autophagy in human gastric cancer cells

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