The effect of 17-allylamino-17-demethoxygeldanamycin alone or in combination with paclitaxel on anaplastic thyroid carcinoma cells

Kim, Si Hyoung; Kang, Jun Goo; Kim, Chul Sik; Ihm, Sung-Hee; Choi, Moon Gi; Yoo, Hyung Joon; Lee, Seong Jin

doi:10.1007/s12020-014-0371-2

Cited by 18 publications

(23 citation statements)

References 23 publications

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“…Meanwhile, in DNA damage response (DDR), Chk1 and p53 play complementary roles in modulating cell cycle after DNA damage, and gH2AX is required for recruiting DDR proteins onto damaged chromatin [25,26]. In this regard, our previous studies showed that NVP-AUY922 and 17-AAG led to downregulation of survivin and upregulation of DDR in ATC cells [7,8]. In the present study, the involvement of survivin and DDR in synergistic activity of BIIB021 with triptolide was identified.…”

Section: The Synergism Between Biib021 and Triptolide Is Associated Wmentioning

confidence: 59%

“…We previously reported that the hsp90 inhibitors NVP-AUY922, 17-AAG and radicicol had a cytotoxic activity in ATC cells [7][8][9]. In the present study, the effect of the hsp90 inhibitor BIIB021 on cell survival and expression of hsp90 client proteins was evaluated in thyroid carcinoma cells.…”

Section: Biib021 Induces Cell Death With Concomitant Alterations In Ementioning

confidence: 81%

“…Hsp90 inhibitors alone or in combination with other chemotherapeutic agents cause cytotoxicity in thyroid carcinoma cells [7][8][9]. In the present study, BIIB021 resulted in death of thyroid carcinoma cells, and thus the effect of BIIB021 in combination with triptolide on survival of thyroid carcinoma cells was evaluated.…”

Section: Biib021 Synergizes With Triptolide In Induction Of Death Of mentioning

confidence: 94%

“…Considering that overexpression of hsp90 is related to poor survival rates in human malignancies, several hsp90 inhibitors as single or combination regimens are currently implicated in cancer patients [5,6]. In this regard, we previously reported that the hsp90 inhibitors NVP-AUY922, 17-allylamino-17-demethoxygeldanamycin (17-AAG) and radicicol alone or in combination with chemotherapeutic agents induced cytotoxicity in ATC cells [7][8][9]. BIIB021 (CNF2024) is a synthetic hsp90 inhibitor used for the clinical treatment of hematologic malignancies and solid tumors [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Synergistic cytotoxicity of BIIB021 with triptolide through suppression of PI3K/Akt/mTOR and NF-κB signal pathways in thyroid carcinoma cells

Kim

Kang

Kim

et al. 2016

Biomedicine & Pharmacotherapy

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Section: The Synergism Between Biib021 and Triptolide Is Associated Wmentioning

confidence: 59%

Section: Biib021 Induces Cell Death With Concomitant Alterations In Ementioning

confidence: 81%

Section: Biib021 Synergizes With Triptolide In Induction Of Death Of mentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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Synergistic cytotoxicity of BIIB021 with triptolide through suppression of PI3K/Akt/mTOR and NF-κB signal pathways in thyroid carcinoma cells

Kim

Kang

Kim

et al. 2016

Biomedicine & Pharmacotherapy

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“…25 In contrast, we recently reported that the hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) antagonized with paclitaxel in induction of cytotoxicity in ATC cells. 26 However, the impact of celastrol in combination with paclitaxel on survival of ATC cells has not been identified.…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic effect of celastrol alone or in combination with paclitaxel on anaplastic thyroid carcinoma cells

et al. 2017

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The influence of celastrol alone or in combination with paclitaxel on survival of anaplastic thyroid carcinoma cells was investigated. In 8505C and SW1736 cells, after treatment of celastrol, cell viability decreased, and cytotoxic activity increased. The protein levels of heat shock protein (hsp) 90, hsp70, Bax, death receptor 5, cleaved caspase-3, cleaved poly (ADP-ribose) polymerase, phospho-extracellular signal-regulated kinase 1/2 (ERK1/2), and phospho-c-Jun N-terminal kinase (JNK) were elevated, and those of Bcl2, phospho-nuclear factor-kappaB (NF-κB), and total and phospho-Akt were reduced. The endoplasmic reticulum stress markers expression and reactive oxygen species production were enhanced. In celastrol-treated cells, N-acetylcysteine increased cell viability and phospho-NF-κB protein levels, and decreased reactive oxygen species production and cytotoxic activity. The protein levels of cyclooxygenase 2, phospho-ERK1/2, phospho-JNK and Bip were diminished. After treatment of both celastrol and paclitaxel, compared with paclitaxel alone, cell viability and the percentage of viable cells were reduced, and death rate and cytotoxic activity were elevated. The protein levels of phospho-ERK1/2, phospho-JNK, Bip, and cyclooxygenase 2, and reactive oxygen species production were enhanced. All of the Combination Index values calculated by Chou-Talalay equation were lower than 1.0, implying the synergism between celastrol and paclitaxel in induction of cell death. In conclusion, our results suggest that celastrol induces cytotoxicity through involvement of Bcl2 family proteins and death receptor, and modulation of phospho-NF-κB, Akt, and mitogen-activated protein kinase in association with endoplasmic reticulum stress and reactive oxygen species production in anaplastic thyroid carcinoma cells. Moreover, celastrol synergizes with paclitaxel in induction of cytotoxicity in anaplastic thyroid carcinoma cells.

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Heat shock protein 90: biological functions, diseases, and therapeutic targets

Wei,

Zhang,

Jia

et al. 2024

MedComm

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Heat shock protein 90 (Hsp90) is a predominant member among Heat shock proteins (HSPs), playing a central role in cellular protection and maintenance by aiding in the folding, stabilization, and modification of diverse protein substrates. It collaborates with various co‐chaperones to manage ATPase‐driven conformational changes in its dimer during client protein processing. Hsp90 is critical in cellular function, supporting the proper operation of numerous proteins, many of which are linked to diseases such as cancer, Alzheimer's, neurodegenerative conditions, and infectious diseases. Recognizing the significance of these client proteins across diverse diseases, there is a growing interest in targeting Hsp90 and its co‐chaperones for potential therapeutic strategies. This review described biological background of HSPs and the structural characteristics of HSP90. Additionally, it discusses the regulatory role of heat shock factor‐1 (HSF‐1) in modulating HSP90 and sheds light on the dynamic chaperone cycle of HSP90. Furthermore, the review discusses the specific contributions of HSP90 in various disease contexts, especially in cancer. It also summarizes HSP90 inhibitors for cancer treatment, offering a thoughtful analysis of their strengths and limitations. These advancements in research expand our understanding of HSP90 and open up new avenues for considering HSP90 as a promising target for therapeutic intervention in a range of diseases.

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The effect of 17-allylamino-17-demethoxygeldanamycin alone or in combination with paclitaxel on anaplastic thyroid carcinoma cells

Cited by 18 publications

References 23 publications

Synergistic cytotoxicity of BIIB021 with triptolide through suppression of PI3K/Akt/mTOR and NF-κB signal pathways in thyroid carcinoma cells

Synergistic cytotoxicity of BIIB021 with triptolide through suppression of PI3K/Akt/mTOR and NF-κB signal pathways in thyroid carcinoma cells

Cytotoxic effect of celastrol alone or in combination with paclitaxel on anaplastic thyroid carcinoma cells

Heat shock protein 90: biological functions, diseases, and therapeutic targets

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