Hyperthermia increases the metastatic potential of murine melanoma

Oliveira-Filho, R.S.; Bevilacqua, Ruy Geraldo; Chammas, Roger

doi:10.1590/s0100-879x1997000800005

Cited by 13 publications

(12 citation statements)

References 7 publications

(5 reference statements)

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“…This study examined an acute cellular response (24 h) following thermal ablation, whether the EMT phenotype observed in this study persists over time remains to be delineated. However, Oliveira-Filho and colleagues have previously demonstrated that hyperthermic treatment of murine B16-F10 melanoma cell lines, although having a short-term negative impact upon cell viability and metastatic lung colonisation in mice, cells that were allowed to recover and injected into mice 13 days following heat shock treatment displayed an enhanced metastatic propensity (Oliveira-Filho et al 1997). This points to a somewhat prolonged enhancement of metastatic phenotype induced by a single heat treatment.…”

Section: Discussionmentioning

confidence: 99%

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Lang

Nguyen

et al. 2012

Cell Stress and Chaperones

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Current cancer therapies including cytotoxic chemotherapy, radiation and hyperthermic therapy induce acute proteotoxic stress in tumour cells. A major challenge to cancer therapeutic efficacy is the recurrence of therapyresistant tumours and how to overcome their emergence. The current study examines the concept that tumour cell exposure to acute proteotoxic stress results in the acquisition of a more advanced and aggressive cancer cell phenotype. Specifically, we determined whether heat stress resulted in an epithelial-to-mesenchymal transition (EMT) and/or the enhancement of cell migration, components of an advanced and therapeutically resistant cancer phenotype. We identified that heat stress enhanced cell migration in both the lung A549, and breast MDA-MB-468 human adenocarcinoma cell lines, with A549 cells also undergoing a partial EMT. Moreover, in an in vivo model of thermally ablated liver metastases of the mouse colorectal MoCR cell line, immunohistological analysis of classical EMT markers demonstrated a shift to a more mesenchymal phenotype in the surviving tumour fraction, further demonstrating that thermal stress can induce epithelial plasticity. To identify a mechanism by which thermal stress modulates epithelial plasticity, we examined whether the major transcriptional regulator of the heat shock response, heat shock factor 1 (HSF1), was a required component. Knockdown of HSF1 in the A549 model did not prevent the associated morphological changes or enhanced migratory profile of heat stressed cells. Therefore, this study provides evidence that heat stress significantly impacts upon cancer cell epithelial plasticity and the migratory phenotype independent of HSF1. These findings further our understanding of novel biological downstream effects of heat stress and their potential independence from the classical heat shock pathway.

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Section: Discussionmentioning

confidence: 99%

Heat stress induces epithelial plasticity and cell migration independent of heat shock factor 1

Lang

Nguyen

et al. 2012

Cell Stress and Chaperones

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“…The positive local response does not necessarily mirror the survival because metastatic potential could be increased. The high-energy heating could increase the blood flow, which promotes the dissemination [33] [34] [35] and could likely produce metastases. Promotion of metastases by hyperthermia was observed in laboratory heating experiments on mammary carcinomas in C3H mice [36], sarcoma in rats [37], and Yoshida tumours [38].…”

Section: How Local Is the Local Treatment?mentioning

confidence: 99%

Heating Preciosity—Trends in Modern Oncological Hyperthermia

Szász¹,

Szász²,

Minnaar³

et al. 2017

OJBIPHY

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The use of hyperthermia as a treatment in oncology is a common topic for debate. Some researchers expect a breakthrough in oncological treatments with hyperthermia, whereas others have disregarded the method. Serious questions concerning hyperthermia have arisen. Should homogeneous (isothermal) or heterogeneous (selective) heating being used? When we use selective heating (heterogeneity), should the entire tumour be targeted or should the malignant cells be individually selected? Does the mechanism involve thermal cell death or thermally-assisted cell death? Is the goal necrosis or apoptosis? Is hyperthermia safe as a monotherapy or does it have to be combined with conventional treatments? When the selection is local, how do we act on disseminated cells that represent a high risk of life threatening metastases? When local heating is the focus, how should it be carried out with measured and controlled? Our objective is to show how precise, selective heat transfer is necessary to remove malignant cells and, consequently, how hyperthermia as part of the immune-oncology can change the game in this promising field of oncological therapies.

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“…The blood-flow will be enhanced, the nutrients supply will be higher and the result is the opposite of our aim. The situation becomes even worse by continuing the high-energy heating: the high blood-flow helps the dissemination [147], [148], [149] and could gain the metastases: Figure 11. With this, we can definitely worsen the survival and the quality of life of the patient.…”

Section: Targeting Complicationsmentioning

confidence: 99%