The combination of curcumin and 5-fluorouracil in cancer therapy

Wei, Yumeng; Yang, Panjing; Cao, Shousong; Zhao, Ling

doi:10.1007/s12272-017-0979-x

Cited by 94 publications

(64 citation statements)

References 139 publications

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“…Although 5-FU itself induces NF-κB, curcumin through suppression of NF-κB and antiapoptosis genes including Bcl-xL has a synergic effect via reduction of chemoresistance (Shakibaei et al, 2013;Shakibaei et al, 2015). Similar results have shown a synergistic effect on NF-κB inhibition by curcumin and 5-FU on other cancer cell types such as esophageal squamous cell carcinoma (Tian, Fan, Zhang, Jiang, & Zhang, 2012;Wei, Yang, Cao, & Zhao, 2018). Curcumin via activation of IκB reduces NF-κB activity in ovarian cancer cell lines, leading to potentiation of apoptosis induction by cisplatin (Fogoros, Choi, & Liu, 2005).…”

Section: Inhibition Of Nf-κbmentioning

confidence: 77%

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mortezaee

Salehi

Mirtavoos-Mahyari

et al. 2019

Journal Cellular Physiology

271

154

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Cancer incidences are growing and cause millions of deaths worldwide. Cancer therapy is one of the most important challenges in medicine. Improving therapeutic outcomes from cancer therapy is necessary for increasing patients’ survival and quality of life. Adjuvant therapy using various types of antibodies or immunomodulatory agents has suggested modulating tumor response. Resistance to apoptosis is the main reason for radioresistance and chemoresistance of most of the cancers, and also one of the pivotal targets for improving cancer therapy is the modulation of apoptosis signaling pathways. Apoptosis can be induced by intrinsic or extrinsic pathways via stimulation of several targets, such as membrane receptors of tumor necrosis factor‐α and transforming growth factor‐β, and also mitochondria. Curcumin is a naturally derived agent that induces apoptosis in a variety of different tumor cell lines. Curcumin also activates redox reactions within cells inducing reactive oxygen species (ROS) production that leads to the upregulation of apoptosis receptors on the tumor cell membrane. Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis. Furthermore, curcumin has a potent inhibitory effect on the activity of NF‐κB and COX‐2, which are involved in the overexpression of antiapoptosis genes such as Bcl‐2. It can also attenuate the regulation of antiapoptosis PI3K signaling and increase the expression of MAPKs to induce endogenous production of ROS. In this paper, we aimed to review the molecular mechanisms of curcumin‐induced apoptosis in cancer cells. This action of curcumin could be applicable for use as an adjuvant in combination with other modalities of cancer therapy including radiotherapy and chemotherapy.

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Section: Inhibition Of Nf-κbmentioning

confidence: 77%

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mortezaee

Salehi

Mirtavoos-Mahyari

et al. 2019

Journal Cellular Physiology

271

154

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“…27,28 However, 5-FU-based therapeutic has limited clinical treatment because of dose-limiting cytotoxicity. 29 Our study still contains certain limitations. Although we discovered the potential diagnostic value of UPP1 in thyroid cancer and related EMT, the specific mechanisms of UPP1 in thyroid cancer remain to be further investigated.…”

Section: Discussionmentioning

confidence: 90%

Uridine phosphorylase 1 associates to biological and clinical significance in thyroid carcinoma cell lines

Guan

Bhandari

Zhang

et al. 2019

J Cellular Molecular Medi

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Thyroid cancer incidence has been continuity increasing worldwide. Uridine phosphorylase 1 (UPP1) is a protein‐coding gene and has been detected that UPP1 was the higher expression in many solid malignancies, just as head and neck cancers, breast cancer, compared with paired normal tissue. But the act of UPP1 in thyroid cancer is not explicit. In this article, we investigate the function of UPP1 expression in thyroid cancer. The Cancer Genome Atlas (TCGA) unpaired thyroid cancer and normal RNA‐seq data were downloaded, and our paired thyroid cancer and normal samples were analysed by a polymerase chain reaction. The expression of UPP1 was regulated by transfected small interfering RNA, and the function of UPP1 was determined via migration, invasion and cell proliferation assays. Western blot assay was achieved to determine the UPP1 expression correlates with the function of 5‐FU regulate epithelial‐mesenchymal transition. The significant upregulation of UPP1 in thyroid cancer tissues compared with normal thyroid tissues was revealed by our data and TCGA data. UPP1 overexpression was significantly correlated with lymph node metastasis, tumour stage and tumour size. In the cell, experiments showed that UPP1 low expression significantly suppressed the migration, invasion and proliferation. Western blot assay proves the effect of UPP1 expression on 5‐FU regulates epithelial‐mesenchymal transition pathway. UPP1 plays a crucial oncogene in thyroid cancer. Our findings indicate that UPP1 might be a biomarker of thyroid cancer and may act by regulating epithelial‐mesenchymal transition (EMT).

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“…Yu et al found that the growth of SMMC-7721 cells could be resisted by CU, which was due to inhibiting the Bcl-2 and activate Bax protein and promote caspase 3 pathway [36]. And some researches also demonstrated that the anticancer effect of 5-FU against cancers could be enhanced by CU via down-regulation of COX-2 and NF-κB pathways [37,38]. Therefore, it may be an ideal strategy to use the combination of CU and 5-FU to treat HCC.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Effects of Curcumin and 5-Fluorouracil on the Hepatocellular Carcinoma In vivo and vitro through regulating the expression of COX-2 and NF-κB

Xu¹,

Guo²,

Pi³

et al. 2020

J. Cancer

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Curcumin (CU) has shown broad anti-cancer effects. 5-fluorouracil (5-FU) has been a conventional chemotherapeutic agent for hepatocellular carcinoma. Unfortunately, the nonspecific cytotoxicity and multidrug resistance caused by long-term use limited the clinical efficacy of 5-FU. This study was aimed to investigate whether the combination of CU and 5-FU could generate synergistic effect in inhibiting the human hepatocellular carcinoma. The results of cytotoxicity test showed that compared with applying single drugs, the combination of CU and 5-FU (1:1, 1:2, 1:4, 2:1 and 4:1, mol/mol) presented stronger cytotoxicity in SMMC-7721, Bel-7402, HepG-2 and MHCC97H cells, while the combination groups are relatively insensitive to normal hepatocytes (L02). Among them, the molar ratio of 2:1 combination group showed strong synergistic effect in SMMC-7721cells. Then, western blotting assay further verified that the mechanism of the synergistic effect may be related to the inhibition of the expression of NF-κB (overall) and COX-2 protein. In addition, the synergistic effect was also validated in the xenograft mice in vivo. This research not only provides a novel and effective combination strategy for the therapy of hepatocellular carcinoma but also provides an experimental basis for the development of CU and 5-FU compound preparation.

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The combination of curcumin and 5-fluorouracil in cancer therapy

Cited by 94 publications

References 139 publications

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy

Uridine phosphorylase 1 associates to biological and clinical significance in thyroid carcinoma cell lines

Synergistic Effects of Curcumin and 5-Fluorouracil on the Hepatocellular Carcinoma In vivo and vitro through regulating the expression of COX-2 and NF-κB

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