Hyperthermia enhances the effect of β-lapachone to cause γH2AX formations and cell death in human osteosarcoma cells

Hori, Takeshi; Kondo, Takashi; Lee, Hyemi; Song, Chang W.; Park, Heon Joo

doi:10.3109/02656736.2010.513361

Cited by 19 publications

(15 citation statements)

References 35 publications

(95 reference statements)

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“…For the physical methods, hyperthermia [74], heat shock [75,76], and photodynamic therapy (PDT) [77] showed synergistic enhancement of antitumor effect of β-lapachone by induction of NQO1 production. Under proper control of β-lapachone dosage and localization of the tumor, these physical methods can be good for βlapachone treatment.…”

Section: The Synergistic Of Drugs With β-Lapachone On Tumorsmentioning

confidence: 99%

The chemotherapeutic effects of lapacho tree extract: β-lapachone

Kung¹,

Lu²,

Chau³

2014

Chemotherapy

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Section: The Synergistic Of Drugs With β-Lapachone On Tumorsmentioning

confidence: 99%

The chemotherapeutic effects of lapacho tree extract: β-lapachone

Kung¹,

Lu²,

Chau³

2014

Chemotherapy

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“…Interestingly, as mentioned above, DMM, DMF, fish oil, 13-cis-retinoic acid, aspirin, and ibuprofen have been reported to upregulate NQO1 [26]. Importantly, various anti-cancer agents such as IR [3-6], chemotherapy drugs [7] and hyperthermia (heat shock) [8-11] and hypoxia (our unpublished observation) also increase NQO1 levels (Fig. 2).…”

Section: Nad(p)h:quinone Oxidoreductasementioning

confidence: 56%

“…β-Lap has been shown to induce apoptosis in various types of cancer cell lines including prostate, lung, pancreas, colon, ovary and breast cancer [1-18]. Furthermore, β-Lap has recently been demonstrated to synergistically interact with IR [3-6] and certain chemotherapy drugs [7] and heat shock [8-11] to kill cancer cells. There have been extensive investigations on the mechanisms of the anti-cancer effects of β-Lap.…”

Section: β-Lapachonementioning

confidence: 99%

“…Importantly, the level of NQO1 activity in many cancers is significantly higher than that in normal tissues indicating that cancer cells are more vulnerable to β-Lap than normal cells. Recent studies clearly demonstrated that β-Lap is not only cytotoxic by itself but it also potentiates the response of cancer cells to ionizing radiation (IR) [3-6], chemotherapy [7], and hyperthermia [8-11]. The purpose of this article is to review recent reports on the molecular mechanisms underlying the anti-cancer effect of β-Lap alone or in combination with ionizing radiation.…”

Section: Introductionmentioning

confidence: 99%

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Enhancement of radiation effect using beta-lapachone and underlying mechanism

et al. 2013

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Beta-lapachone (β-Lap; 3,4-dihydro-2, 2-dimethyl-2H-naphthol[1, 2-b]pyran-5,6-dione) is a novel anti-cancer drug under phase I/II clinical trials. β-Lap has been demonstrated to cause apoptotic and necrotic death in a variety of human cancer cells in vitro and in vivo. The mechanisms underlying the β-Lap toxicity against cancer cells has been controversial. The most recent view is that β-Lap, which is a quinone compound, undergoes two-electron reduction to hydroquinone form utilizing NAD(P)H or NADH as electron source. This two-electron reduction of β-Lap is mediated by NAD(P)H:quinone oxidoreductase (NQO1), which is known to mediate the reduction of many quinone compounds. The hydroquinone forms of β-Lap then spontaneously oxidizes back to the original oxidized β-Lap, creating futile cycling between the oxidized and reduced forms of β-Lap. It is proposed that the futile recycling between oxidized and reduced forms of β-Lap leads to two distinct cell death pathways. First one is that the two-electron reduced β-Lap is converted first to one-electron reduced β-Lap, i.e., semiquinone β-Lap (SQ)·- causing production of reactive oxygen species (ROS), which then causes apoptotic cell death. The second mechanism is that severe depletion of NAD(P)H and NADH as a result of futile cycling between the quinone and hydroquinone forms of β-Lap causes severe disturbance in cellular metabolism leading to apoptosis and necrosis. The relative importance of the aforementioned two mechanisms, i.e., generation of ROS or depletion of NAD(P)H/NADH, may vary depending on cell type and environment. Importantly, the NQO1 level in cancer cells has been found to be higher than that in normal cells indicating that β-Lap may be preferentially toxic to cancer cells relative to non-cancer cells. The cellular level of NQO1 has been found to be significantly increased by divergent physical and chemical stresses including ionizing radiation. Recent reports clearly demonstrated that β-Lap and ionizing radiation kill cancer cells in a synergistic manner. Indications are that irradiation of cancer cells causes long-lasting elevation of NQO1, thereby sensitizing the cells to β-Lap. In addition, β-Lap has been shown to inhibit the repair of sublethal radiation damage. Treating experimental tumors growing in the legs of mice with irradiation and intraperitoneal injection of β-Lap suppressed the growth of the tumors in a manner more than additive. Collectively, β-Lap is a potentially useful anti-cancer drug, particularly in combination with radiotherapy.

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“…shifting of intracellular MRP storage pools, changes in membrane fluidity at the protein level [19]. The application of heating at temperatures above 55 C for 5 min, leads to distinct DNA damages, which cannot be repaired by endogenous DNA repair systems [10] as well as to gamma H2AX foci formation [20], decrease of cellular ATP [21] for example. The intratumoral application of the magnetic material was shown to be an efficient tool for the induction of hyperthermic and thermoablative temperatures in several preclinical studies using laboratory animals.…”

Section: Pros and Cons For Magnetic Hyperthermia After Intratumoral Amentioning

confidence: 99%

In vivo applications of magnetic nanoparticle hyperthermia

Hilger

2013

International Journal of Hyperthermia

154

105

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Hyperthermia is considered to be a promising tool for the treatment of tumours. Intensive research activities reveal a distinct impact not only on the cellular level but also on tumour physiology which favours the combination with the classical oncologic modalities radio- and chemotherapy. Different techniques have been established so far. Among them, magnetic hyperthermia exploits the intrinsic magnetic properties of iron oxide nanoparticles (magnetite and maghemite) which induce heating during the exposure to an alternating magnetic field. Beyond the advantage that heating is generated within the tumour and not from outside the body, the amounts of magnetic material and their intratumoral distribution patterns are key factors determining the therapeutic outcome. They can be influenced by the use of different application routes, which will be discussed in this paper.

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Hyperthermia enhances the effect of β-lapachone to cause γH2AX formations and cell death in human osteosarcoma cells

Cited by 19 publications

References 35 publications

The chemotherapeutic effects of lapacho tree extract: β-lapachone

The chemotherapeutic effects of lapacho tree extract: β-lapachone

Enhancement of radiation effect using beta-lapachone and underlying mechanism

In vivo applications of magnetic nanoparticle hyperthermia

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