Heat Shock Protein Levels Are Not Elevated in Heat-Resistant B16 Melanoma Cells

Anderson, Robin L.; Tao, Tien-Wen; Betten, David A.; Hahn, George M.

doi:10.2307/3576549

Cited by 42 publications

(17 citation statements)

References 14 publications

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“…In some cases, it was reported that the CHX effect on TT expression depended on the test temperature used Dewey, 1987a, 1988). Furthermore, some heat-resistant variants showed elevated HSP levels (Laszlo and Li, 1985;Chretien and Landry, 1988;Landry et al, 1989;Li and Mak, 1989) while others did not (Anderson et al, 1986). Finally, slow rates of heating can cause substantial thermotolerance, with greatly reduced or no detectable HSP synthesis (Tomasovic et al, 1983;Anderson et al, 1988).…”

mentioning

confidence: 99%

Acquisition of thermotolerance induced by heat and arsenite in HeLa S3 cells: Multiple pathways to induce tolerance?

Kampinga

Brunsting

Konings

1992

Journal Cellular Physiology

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Recent data indicate that cells may acquire thermotolerance via more than one route. In this study, we observed differences in thermotolerance development in HeLa S3 cells induced by prior heating (15 minutes at 44 degrees C) or pretreatment with sodium-arsenite (1 hour at 37 degrees C, 100 microM). Inhibition of overall protein and heat shock protein (HSP) synthesis (greater than 95%) by cycloheximide (25 micrograms/ml) during tolerance development nearly completely abolished thermotolerance induced by arsenite, while significant levels of heat-induced thermotolerance were still apparent. The same dependence of protein synthesis was found for resistance against sodium-arsenite toxicity. Toxic heat, but not toxic arsenite treatments caused heat damage in the cell nucleus, measured as an increase in the protein mass of nuclei isolated from treated cells (intranuclear protein aggregation). Recovery from this intranuclear protein aggregation was observed during post-heat incubations of the cells at 37 degrees C. The rate of recovery was faster in heat-induced tolerant cells than in nontolerant cells. Arsenite-induced tolerant cells did not show an enhanced rate of recovery from the heat-induced intranuclear protein aggregation. In parallel, hyperthermic inhibition of RNA synthesis was the same in tolerant and nontolerant cells, whereas post-heat recovery was enhanced in heat-induced, but not arsenite-induced thermotolerant cells. The more rapid recovery from heat damage in the nucleus (protein aggregation and RNA synthesis) in cells made tolerant by a prior heat treatment seemed related to the ability of heat (but not arsenite) to induce HSP translocations to the nucleus.

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mentioning

confidence: 99%

Acquisition of thermotolerance induced by heat and arsenite in HeLa S3 cells: Multiple pathways to induce tolerance?

Kampinga

Brunsting

Konings

1992

Journal Cellular Physiology

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“…Remarkably, whereas heat and BA priming exerted similar protective effects, BA treatment evoked weaker HSP response relative to heat priming at a HSP level. Noteworthy, no major differences were found in the levels of major HSPs between the heat sensitive B16 parent line and the heat resistant variants in other work, suggesting that HSPs are not a determining factor in the heatresistant phenotype of B16 melanoma cells [76]. Thus, the acquired heat tolerance observed in this study should involve other mechanisms (see above) rather than solely the de novo synthesis of HSP chaperones.…”

Section: Acquisition Of Thermotolerance Via Prior Membrane Hyperfluidmentioning

confidence: 61%

Membrane fluidity matters: Hyperthermia from the aspects of lipids and membranes

Csoboz

Balogh

Kúsz

et al. 2013

International Journal of Hyperthermia

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Hyperthermia is a promising treatment modality for cancer in combination both with radio-and chemotherapy. In spite of its great therapeutic potential, the underlying molecular mechanisms still remain to be clarified. Due to lipid imbalances and 'membrane defects' most of the tumour cells possess elevated membrane fluidity. However, further increasing membrane fluidity to sensitise to chemo-or radiotherapy could have some other effects. In fact, hyperfluidisation of cell membrane induced by membrane fluidiser initiates a stress response as the heat shock protein response, which may modulate positively or negatively apoptotic cell death. Overviewing some recent findings based on a technology allowing direct imaging of lipid rafts in live cells and lipidomics, novel aspects of the intimate relationship between the 'membrane stress' of tumour cells and the cellular heat shock response will be highlighted. Our findings lend support to both the importance of membrane remodelling and the release of lipid signals initiating stress protein response, which can operate in tandem to control the extent of the ultimate cellular thermosensitivity. Overall, we suggest that the fluidity variable of membranes should be used as an independent factor for predicting the efficacy of combinational cancer therapies.

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“…Segundo SCHMIDT-NIELSEN (1983) três variáveis podem atuar: 1) as condições de temperatura ambiente em que o animal estava habituado antes da exposição ao calor; 2) as condições gerais do organismo, tais como a quantidade de lí- LINDQUIST & GRAIG (1988) a tolerância térmica é um efeito temporário contra temperaturas letais, induzida por proteínas em células e organismos após um condicionamento térmico a temperaturas intermediárias ou depois do stress provocado principalmente por tratamento com calor. ANDERSON (1986), seguindo a mesma linha experimental, observou células com diferentes níveis de tolerância ao calor, mas sem alteração da síntese de proteínas de resistência a altas temperaturas. ARTMOWIDJOJO et al (1997) estudaram a tolerância a altas temperaturas no deserto do Arizona em A. mellifera e chegaram a um limite de 57ºC atingindo um limite de sobrevivência bem mais elevado do que S. postica que suportou no seu limite extremo 41,5ºC no verão.…”

Section: Discussionunclassified

Capacidade de resistência a altas e baixas temperaturas em operárias de Scaptotrigona postica (Latreille) (Hymenoptera, Apidae) durante os períodos de verão e inverno

Macieira

Proni

2004

Rev. Bras. Zool.

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As abelhas sem ferrão são consideradas por muitos autores de grande importância para o ecossistema devido a sua eficiência como polinizadoras. O presente trabalho estudou a tolerância de operárias de Scaptotrigona postica (Latreille, 1807) à mudanças de temperatura, com o objetivo de determinar os limites térmicos letais (TL - temperatura letal) para altas e baixas temperaturas durante o verão e inverno. Os resultados mostraram um intervalo de tolerância entre -3,5ºC e 40ºC no verão e de -4,0 até 39,5ºC no inverno a 50% de sobrevivência de uma população (LT50). Os limites a 100% de mortalidade (LT100) foram entre -5ºC e 41ºC no verão e -5ºC e 40,5ºC no inverno.

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Heat Shock Protein Levels Are Not Elevated in Heat-Resistant B16 Melanoma Cells

Cited by 42 publications

References 14 publications

Acquisition of thermotolerance induced by heat and arsenite in HeLa S3 cells: Multiple pathways to induce tolerance?

Acquisition of thermotolerance induced by heat and arsenite in HeLa S3 cells: Multiple pathways to induce tolerance?

Membrane fluidity matters: Hyperthermia from the aspects of lipids and membranes

Capacidade de resistência a altas e baixas temperaturas em operárias de Scaptotrigona postica (Latreille) (Hymenoptera, Apidae) durante os períodos de verão e inverno

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