Short-Term Hyperthermia Promotes the Sensitivity of MCF-7 Human Breast Cancer Cells to Paclitaxel

Yc, Lin; Liu, Zhihui; Li, Yongqiang; Liao, Sina; Cen, Shaofang; Yang, Ling; Wei, Jiazhang; Hu, Xiaohua

doi:10.1248/bpb.b12-00774

Cited by 9 publications

(10 citation statements)

References 26 publications

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“…Analysis of cell cycle revealed increased presence of HT29 cells in G 2 /M phase after heat shock application, while combination of hyperthermia with auraptene resulted in considerable accumulation of cells in sub G 1 /G 1 phase. In consistence with our findings, G 2 /M phase arrest was reported after hyperthermia in several cell types such as liver, lung, breast and renal cancer cells (Qi et al 2015;Zhao et al 2015;Yan et al 2014;Lin et al 2013). Same as present results, previous studies have also indicated growth controlling effects of auraptene on breast and gastric carcinoma cells by cell cycle arrest in sub G 1 (Mousavi et al 2015, Moon et al 2015 and G 0 -G 1 phases (de Medina et al 2010;Krishnan et al 2009).…”

Section: R a F Tsupporting

confidence: 91%

Efficacy of hyperthermia in human colon adenocarcinoma cells is improved by auraptene

Moussavi

Haddad

Matin

et al. 2018

Biochem. Cell Biol.

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Colon adenocarcinoma is one of the most common cancers worldwide, and resistance to current therapeutic modalities is a serious drawback in its treatment. Auraptene is a natural coumarin with considerable anticancer effects. The goal of this study was to introduce a novel combinatorial approach for treatment against colon adenocarcinoma cells. To do so, HT29 cells were pretreated with nontoxic auraptene and then hyperthermia was induced. Afterwards, the viability of the cells was assessed, changes induced in the cell cycle were analyzed, and the expression patterns of candidate genes were studied. Results from the MTT assay demonstrated significant (p < 0.01) decreases in cell viability when 20 μg/mL auraptene was used for 72 h, heat shock was induced, and cells were allowed to recover for 24 h. Flow cytometry analysis also indicated considerable changes in the distribution of cells between the sub-G/G and G/M phases of cell cycle after the combinatorial treatment. Real-time RT-PCR studies revealed significant (p < 0.01) up-regulation of P21 in the cells pretreated with auraptene after heat shock, whereas no significant change was observed in HSP27 expression. Our findings not only indicate, for the first time, that the efficacy of hyperthermia was improved by auraptene pretreatment, but also suggest that this coumarin could be used in the future to achieve more effective therapeutic outcomes.

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Section: R a F Tsupporting

confidence: 91%

Efficacy of hyperthermia in human colon adenocarcinoma cells is improved by auraptene

Moussavi

Haddad

Matin

et al. 2018

Biochem. Cell Biol.

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“…31,37,39,50,51 Both in vitro and in vivo studies proved that this combination induced a "thermal enhancement" for PTX cytotoxicity. 31,50,51 In current clinical trials, PTX is administered with hyperthermic perfusion for the treatment of ovarian and lung cancers and gastrointestinal neoplasms (http://www.clinicaltrial.gov).…”

Section: Discussionmentioning

confidence: 95%

“…Physiological hyperthermia (39.5-45 °C) has been used as enhancer of radiotherapy and of many chemotherapeutic agents, 30 including PTX, [31][32][33] with limited toxicity to normal tissues. 34 Hyperthermia is mainly applied locally, regionally, interstitially, or to the whole body according to the tumor type, stage, depth, localization, and presence of spread metastatic disease.…”

Section: Introductionmentioning

confidence: 99%

“…36 Another reason for the hesitancy toward the use of hyperthermia, alone or as PTX sensitizer, can be attributed to conflicting outcomes of preclinical studies. 31,[37][38][39] However, these differences can be explained by the substantial variations in the HT protocols applied (e.g., temperature, length of HT treatment, concentration, and length of PTX exposure).…”

Section: Introductionmentioning

confidence: 99%

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Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

et al. 2013

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Microtubule-poisoning drugs, such as Paclitaxel (or taxol, PtX), are powerful and commonly used anti-neoplastic agents for the treatment of several malignancies. PtX triggers cell death, mainly through a mitotic arrest following the activation of the spindle assembly checkpoint (SAC). Cells treated with PtX slowly slip from this mitotic block and die by mitotic catastrophe. However, cancer cells can acquire or are intrinsically resistant to this drug, posing one of the main obstacles for PtX clinical effectiveness. In order to override PtX resistance and increase its efficacy, we investigated both the enhancement of mitotic slippage and the block of mitotic exit.to test these opposing strategies, we used physiological hyperthermia (Ht) to force exit from PtX-induced mitotic block and the anaphase-promoting complex/cyclosome (APC/C) inhibitor, protAMe, to block mitotic exit. We observed that application of Ht on PtX-treated cells forced mitotic slippage, as shown by the rapid decline of cyclin B levels and by microscopy analysis. Similarly, Ht induced mitotic exit in cells blocked in mitosis by other antimitotic drugs, such as Nocodazole and the Aurora A inhibitor MLN8054, indicating a common effect of Ht on mitotic cells. On the other hand, protAMe prevented mitotic exit of PtX and MLN8054 arrested cells, prolonged mitosis, and induced apoptosis. In addition, we showed that protAMe prevented Ht-mediated mitotic exit, indicating that stress-induced APC/C activation is necessary for Ht-induced mitotic slippage.Finally, Ht significantly increased PtX cytotoxicity, regardless of cancer cells' sensitivity to PtX, and this activity was superior to the combination of PtX with pro-tAMe. Our data suggested that forced mitotic exit of cells arrested in mitosis by anti-mitotic drugs, such as PtX, can be a more successful anticancer strategy than blocking mitotic exit by inactivation of the APC/C.

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“…HT is reported to be a good strategy for cancer both by itself [1] and in conjunction with radiotherapy or chemotherapy [38, 39]. In addition, it is now considered a potential tool for treating cancer after surgery, radiotherapy, and chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Baicalin Augments Hyperthermia-Induced Apoptosis in U937 Cells and Modulates the MAPK Pathway via ROS Generation

Zakki

Cui

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hyperthermia is a widely used therapeutic tool for cancer therapy and a well-known inducer of apoptosis. Although the flavonoid compound baicalin (BCN) is a potent anticancer agent for several human carcinomas, it is less potent in the human U937 myelomonocytic leukemia cell line. To explore any enhancing effects of BCN on hyperthermia-induced apoptosis, this study investigated the combined effects and apoptotic mechanisms of hyperthermia and BCN in U937 cells. Methods: U937 cells were heat treated at 44ºC for 12 min with or without pre-treatment with BCN (10-50 µM) and then incubated for 6 h at 37 ºC with 5% CO₂ and 95% air. Cell viability was analyzed by Trypan blue exclusion assay. Apoptosis was examined by DNA fragmentation, fluorescence microscopy and flow cytometry. Generation of mitochondrial trans-membrane potential (MMP), mitochondrial calcium, and reactive oxygen species (ROS) was also detected by flow cytometry. The expression of proteins related to apoptosis and signaling pathways was determined by western blotting. Results: Hyperthermia alone did not reduce cell viability or induce notable levels of apoptosis, but combined hyperthermia and BCN treatment markedly augmented apoptosis by upregulating proapoptotic proteins and suppressing antiapoptotic proteins, culminating in caspase-3 activation. Mitochondrial transmembrane potential was significantly decreased, and generation of reactive oxygen species (ROS) and suppression of antioxidant enzymes were marked. Furthermore, with the combined treatment, the phosphorylated forms of JNK and p38 showed increased expression, whereas AKT was dephosphorylated. JNK-IN-8 (a JNK inhibitor) and NAC (a ROS scavenger) abrogated the apoptotic effects of the combined treatment, significantly protecting the cells and indicating the involvement of high ROS generation and the MAPK pathway in the underlying molecular mechanism. Conclusion: This study provides compelling evidence that hyperthermia, in combination with BCN, is a promising therapeutic strategy for enhancement of apoptosis and suggest a promising therapeutic approach for cancer.

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Short-Term Hyperthermia Promotes the Sensitivity of MCF-7 Human Breast Cancer Cells to Paclitaxel

Cited by 9 publications

References 26 publications

Efficacy of hyperthermia in human colon adenocarcinoma cells is improved by auraptene

Efficacy of hyperthermia in human colon adenocarcinoma cells is improved by auraptene

Targeting mitotic exit with hyperthermia or APC/C inhibition to increase paclitaxel efficacy

Baicalin Augments Hyperthermia-Induced Apoptosis in U937 Cells and Modulates the MAPK Pathway via ROS Generation

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