Nutraceutical Boom in Cancer: Inside the Labyrinth of Reactive Oxygen Species

Calvani, Maura; Pasha, Amada; Favre, Claudio

doi:10.3390/ijms21061936

Cited by 71 publications

(43 citation statements)

References 173 publications

(175 reference statements)

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“…Reduced levels of nonenzymatic antioxidants were observed in oral carcinogenesis. [ 36 ] Declined levels of GSH and vitamin E in the plasma of OSCC models propose that these antioxidants are exploited by carcinoma to achieve the nutrient requirement for growing tumor volume or to combat the detrimental effects of ROS. [ 37 ] Suppressed enzymatic antioxidants' activities are presumably due to their debilitation in deducing LHPOs' exhilarated levels.…”

Section: Discussionmentioning

confidence: 99%

Anticancer activity of Vicenin‐2 against 7,12 dimethylbenz[a]anthracene‐induced buccal pouch carcinoma in hamsters

Zheng

Wang³

2020

J Biochem & Molecular Tox

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Buccal mucosa carcinoma is a significant cause of death in developing nations. Vicenin‐2 is a significant bioactive compound found in Ocimum sanctum Linn or Tulsi that possesses several pharmacologic properties. Our focus is to understand the possible impact of Vicenin‐2 on 7,12‐dimethylbenz[a]anthracene (DMBA)‐induced oral carcinogenesis in hamsters. Buccal carcinoma was induced by treatment with carcinogenic DMBA, three times a week for 14 weeks. We determined 100% tumor incidence, abnormal tumor volume, inclined tumor burden, and deduced body weight in DMBA‐induced oral squamous cell carcinoma (OSCC) hamsters. The upregulation of cytokine levels (interleukin [IL]‐6, IL‐1β, and tumor necrosis factor‐alpha [TNF‐α]) was observed in DMBA‐induced OSCC hamsters. Moreover, dysplastic, hyperplastic, and squamous cell carcinoma was identified in the DMBA‐induced OSCC hamsters. The diminished activities of lipid peroxidation and enzymatic/nonenzymatic antioxidants were observed in DMBA‐induced hamsters. Furthermore, the high expression of proliferating cell nuclear antigen (PCNA), Cyclin‐D1, and Bcl‐2, and attenuated Bax expression were observed in DMBA‐induced hamsters. Our study results explored that Vicenin‐2 (30 mg/kg) treated with DMBA‐brushed hamsters averted tumor incidence, improved the antioxidant status, and inhibited lipid peroxidation. Moreover, Vicenin‐2 inhibited the immunohistochemical expression of PCNA, Cyclin‐D1, and Bcl‐2, and significantly restored apoptotic Bax levels. The Vicenin‐2 treatment prevents the lesion formation in the oral epithelium of the DMBA‐induced hamsters. The Vicenin‐2 treatment potentially halts the proinflammatory cytokines (IL‐6, IL‐1β, and TNF‐α) production in OSCC hamsters. Thus, we proved that Vicenin‐2 prevents DMBA‐induced buccal carcinogenesis in hamsters via improving antioxidants by modulating apoptotic and cytokines signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Anticancer activity of Vicenin‐2 against 7,12 dimethylbenz[a]anthracene‐induced buccal pouch carcinoma in hamsters

Zheng

Wang³

2020

J Biochem & Molecular Tox

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“…Different nutraceuticals are efficient as adjuvant agents for cancer therapy in in-vivo and in-vitro studies [ 230 , 231 , 232 , 233 ]. A diet abundant in vegetables and fruits is related to cancer risk reduction; however, the mechanisms are still unclear.…”

Section: Csc-targeting Therapeutic Approachesmentioning

confidence: 99%

The Great Escape: The Power of Cancer Stem Cells to Evade Programmed Cell Death

Castelli

Giordano

Benedetti

et al. 2021

Cancers

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Cancer is one of the primary causes of death worldwide. Tumour malignancy is related to tumor heterogeneity, which has been suggested to be due to a small subpopulation of tumor cells named cancer stem cells (CSCs). CSCs exert a key role in metastasis development, tumor recurrence, and also epithelial–mesenchymal transition, apoptotic resistance, self-renewal, tumorigenesis, differentiation, and drug resistance. Several current therapies fail to eradicate tumors due to the ability of CSCs to escape different programmed cell deaths. Thus, developing CSC-selective and programmed death-inducing therapeutic approaches appears to be of primary importance. In this review, we discuss the main programmed cell death occurring in cancer and the promising CSC-targeting agents developed in recent years. Even if the reported studies are encouraging, further investigations are necessary to establish a combination of agents able to eradicate CSCs or inhibit their growth and proliferation.

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“…In general, nutraceuticals are food or food compounds that play a role in maintaining normal physiological functions [ 10 , 11 ]. In cancer, nutraceuticals have the potential to reduce cancer cell growth, inhibit cell proliferation and induce cancer cell apoptosis as many natural and dietary products have been shown to exhibit anti-cancer characteristics [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Anti-Cancer Properties of Theaflavins

et al. 2021

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Cancer is a disease characterized by aberrant proliferative and apoptotic signaling pathways, leading to uncontrolled proliferation of cancer cells combined with enhanced survival and evasion of cell death. Current treatment strategies are sometimes ineffective in eradicating more aggressive, metastatic forms of cancer, indicating the need to develop novel therapeutics targeting signaling pathways which are essential for cancer progression. Historically, plant-derived compounds have been utilized in the production of pharmaceuticals and chemotherapeutic compounds for the treatment of cancer, including paclitaxel and docetaxel. Theaflavins, phenolic components present in black tea, have demonstrated anti-cancer potential in cell cultures in vitro and in animal studies in vivo. Theaflavins have been shown to inhibit proliferation, survival, and migration of many cancer cellswhile promoting apoptosis. Treatment with theaflavins has been associated with increased levels of cleaved poly (ADP-ribose) polymerase (PARP) and cleaved caspases-3, -7, -8, and -9, all markers of apoptosis, and increased expression of the proapoptotic marker Bcl-2-associated X protein (Bax) and concomitant reduction in the antiapoptotic marker B-cell lymphoma 2 (Bcl-2). Additionally, theaflavin treatment reduced phosphorylated Akt, phosphorylated mechanistic target of rapamycin (mTOR), phosphatidylinositol 3-kinase (PI3K), and c-Myc levels with increased expression of the tumour suppressor p53. This review summarizes the current in vitro and in vivo evidence available investigating the anti-cancer effects of theaflavins across various cancer cell lines and animal models.

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Nutraceutical Boom in Cancer: Inside the Labyrinth of Reactive Oxygen Species

Cited by 71 publications

References 173 publications

Anticancer activity of Vicenin‐2 against 7,12 dimethylbenz[a]anthracene‐induced buccal pouch carcinoma in hamsters

Anticancer activity of Vicenin‐2 against 7,12 dimethylbenz[a]anthracene‐induced buccal pouch carcinoma in hamsters

The Great Escape: The Power of Cancer Stem Cells to Evade Programmed Cell Death

Anti-Cancer Properties of Theaflavins

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