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Inhibition of Heme Oxygenase-1 enhances hyperthermia-induced autophagy and antiviral effect.


ABSTRACT: Hyperthermia has been clinically utilized as an adjuvant therapy in the treatment of cervical carcinoma. However, thermotolerance induced by heme oxygenase-1 (HO-1), a stress-inducible cytoprotective protein, limits the efficacy of hyperthermic therapy, for which the exact mechanism remains unknown. In the present study, we found that heat treatment induced HO-1 expression and decreased copy number of HPV16 in cervical cancer cells and tissues from cervical cancer and precursor lesions. Knockdown of HO-1 stimulated autophagy accompanied by downregulation of X-linked inhibitor of apoptosis protein. Furthermore, silencing of HO-1 led to cell intolerance to hyperthermia, as manifested by inhibition of cell viability and induction of autophagic apoptosis. Moreover, HO-1 modulated hyperthermia-induced, autophagy-dependent antiviral effect. Thus, the findings indicate that blockade of HO-1 enhances hyperthermia-induced autophagy, an event resulting in apoptosis of cervical cancer cells through an antiviral mechanism. These observations imply the potential clinical utility of hyperthermia in combination with HO-1 inhibition in the treatment of cervical cancer.

SUBMITTER: Yang Y 

PROVIDER: S-EPMC6367586 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Inhibition of Heme Oxygenase-1 enhances hyperthermia-induced autophagy and antiviral effect.

Yang Yang Y   Wang He-Xiao HX   Zhang Lan L   Huo Wei W   Li Xiao-Dong XD   Qi Rui-Qun RQ   Song Xiao-Yu XY   Wei Shi S   Gao Xing-Hua XH   Han Shuai S   Cao Liu L  

International journal of biological sciences 20190101 3


Hyperthermia has been clinically utilized as an adjuvant therapy in the treatment of cervical carcinoma. However, thermotolerance induced by heme oxygenase-1 (HO-1), a stress-inducible cytoprotective protein, limits the efficacy of hyperthermic therapy, for which the exact mechanism remains unknown. In the present study, we found that heat treatment induced HO-1 expression and decreased copy number of HPV16 in cervical cancer cells and tissues from cervical cancer and precursor lesions. Knockdow  ...[more]

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