Apoptosis: Escaping strategies in human skin cancer (Review)

Giannetti, Luca; Consolo, Ugo; Magnoni, Cristina; Muzio, Lorenzo Lo

doi:10.3892/or.11.2.401

Cited by 11 publications

(11 citation statements)

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“…Previous data have revealed that survivin is one of the genes most consistently over-expressed in tumor cells and plays important roles in both cell proliferation and cell death (30). Downregulation of survivin expression may lead to programmed cell death (31), indicating that it may be an appealing new target for novel therapy in cancer (32). Our results show that tanshinone IIA may trigger apoptosis in COC1/DDP cells by downregulating survivin levels via activation of p38 MAPK.…”

Section: Discussionmentioning

confidence: 55%

Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells

Wen

2011

Oncol Rep

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Abstract. Tanshinone IIA is known to induce apoptosis in several types of cancer cells. However, little is known about its activity in chemoresistant cells. The aim of this study was to investigate the anticancer properties of tanshinone IIA in cisplatin-resistant human ovarian cancer COC1/DDP cells in vitro. We used a variety of methods to measure cell viability, the resistance index (RI) of cisplatin, cellular apoptosis, p38 mitogen-activated protein kinase (MAPK) expression and phosphorylation, and the mRNA expression of several genes implicated in drug resistance including survivin, Caspase-3, excision repair cross-complementing gene 1 (ERCC1), multidrug resistance (MDR), lung resistance protein (LRP) and glutathione-S-transferase-π (GST-π). We found that tanshinone IIA time-and dose-dependently inhibited the proliferation of COC1/DDP cells and caused significant apoptosis. Western blotting revealed that tanshinone IIA also increased phospho-p38 MAPK in a time-and dose-dependent manner. After treatment by tanshinone IIA for 48 h, the RI of cisplatin and the mRNA expression of survivin, ERCC1 and LRP were all significantly decreased. Furthermore, blockade of p38 signal transduction decreased apoptotic cell rates and dramatically elevated the mRNA expression of the survivin, ERCC1 and LRP genes. We therefore conclude that tanshinone IIA induces apoptosis and reduces cisplatin resistance in COC1/DDP cells and thus causes significant growth inhibitory effects. This mechanism appears to involve p38-mediated downregulation of survivin, ERCC1 and LRP mRNA expression.

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Section: Discussionmentioning

confidence: 55%

Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells

Wen

2011

Oncol Rep

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“…Previous data have revealed that survivin is one of the genes most consistently overexpressed in tumor cells which plays important roles in both cell proliferation and cell death (30), down-regulation of survivin expression may lead to programmed cell death (31), indicating that survivin may be an appealing new target for novel therapy in cancer (32). Our results showed that Tanshinone IIA may trigger apoptosis on THP-1 cells via activation of caspase-3 and down-regulation of anti-apoptosis protein Bcl-2 and survivin levels.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA inhibits leukemia THP-1 cell growth by induction of apoptosis

Liu

Zhang²,

Lin³

et al. 2009

Oncol Rep

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Abstract. Tanshinone IIA, a diterpene quinone extracted from the traditional herbal medicine, Salvia miltiorrhiza Bunge, has been reported to have anti-tumor effects on a large variety of cancer cells. The present study was undertaken to investigate the in vitro antiproliferation and apoptosis inducing effects of Tanshinone IIA on leukemia THP-1 cell lines and its mechanisms of action. MTT assay was used to detect the cell growth inhibitory rate; cell apoptotic rate and the mitochondrial membrane potential (Δψm) were investigated by flow cytometry (FCM), apoptotic morphology was observed by Hoechst 33258 staining and DNA fragmentation analysis. The expression of caspase-3 and different apoptosis modulators were analyzed by Western blotting. The results revealed that Tanshinone IIA inhibited the growth of THP-1 cells and caused significant apoptosis, the suppression was both in time-and dose-dependent manner. After treatment by Tanshinone IIA for 48 h, the percentage of disruption of Δψm gradually increased in a dose-dependent manner along with marked changes of cell apoptosis. Western blotting showed cleavage of the caspase-3 zymogen protein (32-kDa) with the appearance of its 20-kDa subunit and a dose-dependent cleavage of PARP, with the appearance of 89-kDa fragment; The expression of Bcl-2 and survivin was down-regulated remarkably while Bax expression was up-regulated concurrently after the cells were treated with Tanshinone IIA for 48 h. We therefore conclude that Tanshinone IIA has significant growth inhibition effects on THP-1 cells by induction of apoptosis, and that Tanshinone IIA-induced apoptosis on THP-1 cells is mainly related to the disruption of Δψm and activation of caspase-3 as well as down-regulation of anti-apoptotic protein Bcl-2, survivin and up-regulation of pro-apoptotic protein Bax. The results indicate that Tanshinone IIA may serve as a potential anti-leukemia reagent.

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“…Mutações neste gene, responsável pela manutenção da integridade genômica por bloquear a replicação do DNA em resposta a danos, ou induzir seu reparo 55 , reduzem sua capacidade em disparar a morte programada de célu-las (apoptose), resultando em maior proliferação celular 56 . Sugerese ainda que, independentemente dos danos causados ao DNA, o desequilíbrio redox provocado pela radiação UV pode interferir na apoptose [57][58][59] . Assim, os efeitos deletérios da radiação UV na pele são cada vez mais evidentes.…”

Section: Alterações Redox Mediadas Pela Exposição Solarunclassified

Antioxidantes na manutenção do equilíbrio redox cutâneo: uso e avaliação de sua eficácia

Guaratini¹,

Medeiros²,

Colepicolo³

2007

Quím. Nova

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Recebido em 12/12/05; aceito em 13/2/06; pleblicado na web em 30/8/06 ANTIOXIDANTS IN THE SKIN: APPLICATIONS AND EVALUATION OF THEIR EFFICACY. The skin is a very complex organ, continuously exposed to physical, chemical and microbiological agents. Enzymes as well as low-molecular weight antioxidants are present in the cutaneous tissue to counterbalance the deleterious effect caused by an oxidative stress and thus maintain homeostasis. Antioxidants such as vitamins C and E, carotenoids, and extracts with these properties have been extensively used for treatment of pathologies and skin aging prevention. We review here different mechanisms that can interfere in the redox equilibrium of the skin, as well as the chemical reactions involved in these processes. Moreover, we discuss the importance of endogenous or exogenous antioxidants that can be acquired from the diet or from oral or topical administration, and methodologies that have been developed to evaluate their efficacy Keywords: skin, antioxidants; efficacy. INTRODUÇÃOA pele é um órgão complexo, formado por diferentes estruturas e com diversos tipos celulares (Figura 1), que atua como uma barreira protetora dos órgãos internos ao ambiente, enquanto mantém o balanço entre proliferação e descamação celular 1 . Mais que qualquer outro tecido, é exposta a inúmeros agentes químicos, físi-cos e microbiológicos, muitos dos quais induzem à formação de espécies reativas de oxigênio (ERO) e de nitrogênio (ERN). Estas espécies são fundamentais em diversos processos fisiopatológicos e bioquímicos, mantendo a sobrevivência e a homeostase celular, sendo que há um equilíbrio refinado entre sua formação e remoção. Porém, quando há alterações acentuadas neste equilíbrio, um estado pró-oxidante é gerado, levando assim ao chamado estresse oxidativo 2 .Neste contexto, fica claro que a pele, por sua importância, é um órgão cujas células possuem mecanismos enzimáticos de resposta rápida, bem como moléculas antioxidantes de baixo peso molecular para contrabalançar o efeito deletério causado por um estresse oxidativo

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Apoptosis: Escaping strategies in human skin cancer (Review)

Cited by 11 publications

References 0 publications

Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells

Tanshinone IIA acts via p38 MAPK to induce apoptosis and the down-regulation of ERCC1 and lung-resistance protein in cisplatin-resistant ovarian cancer cells

Tanshinone IIA inhibits leukemia THP-1 cell growth by induction of apoptosis

Antioxidantes na manutenção do equilíbrio redox cutâneo: uso e avaliação de sua eficácia

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