Vitamin E Analog α -TEA, Methylseleninic Acid, and<i>Trans</i>-Resveratrol in Combination Synergistically Inhibit Human Breast Cancer Cell Growth

Snyder, Rachel M.; Yu, Weiping; Li, Jia; Sanders, Bob G.; Kline, Kimberly

doi:10.1080/01635580701759716

Cited by 9 publications

(4 citation statements)

References 32 publications

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“…During the development of TRG in the early 1990s, an intact α-tocopherol (Vitamin E) moiety was incorporated to avoid lipid peroxidation in the liver [ 141 ]. Analogues of Vitamin E have the capacity to induce apoptosis and synergize with other anticancer agents to inhibit the growth of breast cancer cells in vitro [ 142 , 143 ]. Furthermore, Vitamin E metabolites possess structural qualities that suggest HDACi activity [ 144 ].…”

Section: Reversal Of Mdrmentioning

confidence: 99%

Development, Maintenance, and Reversal of Multiple Drug Resistance: At the Crossroads of TFPI1, ABC Transporters, and HIF1

Arnason

Harkness

2015

Cancers

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Early detection and improved therapies for many cancers are enhancing survival rates. Although many cytotoxic therapies are approved for aggressive or metastatic cancer; response rates are low and acquisition of de novo resistance is virtually universal. For decades; chemotherapeutic treatments for cancer have included anthracyclines such as Doxorubicin (DOX); and its use in aggressive tumors appears to remain a viable option; but drug resistance arises against DOX; as for all other classes of compounds. Our recent work suggests the anticoagulant protein Tissue Factor Pathway Inhibitor 1α (TFPI1α) plays a role in driving the development of multiple drug resistance (MDR); but not maintenance; of the MDR state. Other factors; such as the ABC transporter drug efflux pumps MDR-1/P-gp (ABCB1) and BCRP (ABCG2); are required for MDR maintenance; as well as development. The patient population struggling with therapeutic resistance specifically requires novel treatment options to resensitize these tumor cells to therapy. In this review we discuss the development, maintenance, and reversal of MDR as three distinct phases of cancer biology. Possible means to exploit these stages to reverse MDR will be explored. Early molecular detection of MDR cancers before clinical failure has the potential to offer new approaches to fighting MDR cancer.

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Section: Reversal Of Mdrmentioning

confidence: 99%

Development, Maintenance, and Reversal of Multiple Drug Resistance: At the Crossroads of TFPI1, ABC Transporters, and HIF1

Arnason

Harkness

2015

Cancers

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“…Mechanisms whereby α-TEA induces tumor cells to undergo apoptosis include activation of both death receptors (Fas and DR5) and JNK/p73/Noxa pro-apoptotic pathways; as well as suppression of anti-apoptotic mediators Akt, ERK, c-FLIP and survivin [15,16,18,20,21,28,29]. However, less is known about initiating events that lead to these desirable dual activities.…”

Section: Discussionmentioning

confidence: 99%

α-TEA-induced death receptor dependent apoptosis involves activation of acid sphingomyelinase and elevated ceramide-enriched cell surface membranes

Tiwary

et al. 2010

Cancer Cell Int

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BackgroundAlpha-tocopherol ether-linked acetic acid (α-TEA), an analog of vitamin E (RRR-alpha-tocopherol), is a potent and selective apoptosis-inducing agent for human cancer cells in vivo and in vitro. α-TEA induces apoptosis via activation of extrinsic death receptors Fas (CD95) and DR5, JNK/p73/Noxa pathways, and suppression of anti-apoptotic mediators Akt, ERK, c-FLIP and survivin in breast, ovarian and prostate cancer cells.ResultsIn this study, we demonstrate that α-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells. α-TEA treatment leads to increased acid sphingomyelinase (ASMase) activity by 30 min, peaking at 4 hrs, which is correlated with ASMase translocation from cytosol to the cell surface membrane. Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces α-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in α-TEA-induced apoptosis. Consistent with cell culture data, immunohistochemical analyses of tumor tissues taken from α-TEA treated nude mice bearing MDA-MB-231 xenografts show increased levels of cell surface membrane ceramide in comparison to tumor tissues from control animals.ConclusionTaken together, these studies demonstrate that ASMase activation and membrane ceramide accumulation are early events contributing to α-TEA-induced apoptosis in vitro and perhaps in vivo.

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“…Resveratrol (3,4′,5-trihydroxy-trans-stilbene), a non-flavonoid polyphenol, is a phytoestrogen that attracts significant attention from researchers for its potent effects of anti-oxidant, anti-inflammatory, and anticancer properties in many cancers [59,60,61]. In addition, it is more striking in reversing drug resistance and the sensitizing of cancer cells for chemotherapy and radiotherapy [62,63]. However, it is a pity to know that the poor water solubility and rapid metabolism of RES in the intestine and liver results in low bioavailability of less than 1% which hinders its pharmacological potential [64,65,66].…”

Section: Phytochemicals Conjugated With Nps As Nanomedicinementioning

confidence: 99%

Phytofabrication of Nanoparticles as Novel Drugs for Anticancer Applications

Wei

Chen

et al. 2019

Molecules

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Cancer is one of the foremost causes of death globally and also the major stumbling block of increasing life expectancy. Although the primary treatment of surgical resection, chemotherapy, and radiotherapy have greatly reduced the mortality of cancer, the survival rate is still low because of the metastasis of tumor, a range of adverse drug reactions, and drug resistance. For all this, it is relevant to mention that a growing amount of research has shown the anticarcinogenic effect of phytochemicals which can modulate the molecular pathways and cellular events include apoptosis, cell proliferation, migration, and invasion. However, their pharmacological potential is hindered by their low water solubility, low stability, poor absorption, and rapid metabolism. In this scenario, the development of nanotechnology has created novel formulations to maximize the potential use of phytochemicals in anticancer treatment. Nanocarriers can enhance the solubility and stability of phytochemicals, prolong their half-life in blood and even achieve site-targeting delivery. This review summarizes the advances in utilizing nanoparticles in cancer therapy. In particular, we introduce several applications of nanoparticles combined with apigenin, resveratrol, curcumin, epigallocatechin-3-gallate, 6-gingerol, and quercetin in cancer treatment.

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Vitamin E Analog α -TEA, Methylseleninic Acid, andTrans-Resveratrol in Combination Synergistically Inhibit Human Breast Cancer Cell Growth

Cited by 9 publications

References 32 publications

Development, Maintenance, and Reversal of Multiple Drug Resistance: At the Crossroads of TFPI1, ABC Transporters, and HIF1

Development, Maintenance, and Reversal of Multiple Drug Resistance: At the Crossroads of TFPI1, ABC Transporters, and HIF1

α-TEA-induced death receptor dependent apoptosis involves activation of acid sphingomyelinase and elevated ceramide-enriched cell surface membranes

Phytofabrication of Nanoparticles as Novel Drugs for Anticancer Applications

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