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Targeting Autophagy to Overcome Human Diseases
Article

Differential Involvement of Autophagy and Apoptosis in Response to Chemoendocrine and Endocrine Therapy in Breast Cancer: JBCRG-07TR

1
Breast Surgical Oncology, Breast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo 135-8550, Japan
2
Department of Surgery, Breast Oncology, NHO Osaka National Hospital, Osaka 540-0006, Japan
3
Department of Breast Surgery Sakai Municipal Hospital, Osaka 593-8304, Japan
4
Department of Breast Surgery Yao Municipal Hospital, Osaka 581-0069, Japan
5
Department of Medical Oncology, Fukushima Medical University, Fukushima 960-1247, Japan
6
Department of Breast Surgery, Kyorin University Hospital, Tokyo 181-8611, Japan
7
Department of Pathology, Tohoku University School of Medicine, Sendai 103-0023, Japan
8
Department of Surgery (Breast Surgery), Kyoto University, Kyoto 606-8507, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(4), 984; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040984
Received: 7 February 2019 / Accepted: 21 February 2019 / Published: 24 February 2019
Endocrine therapy is an essential component in the curative treatment of hormone receptor (HR)-positive breast cancer. To improve treatment efficacy, the addition of metronomic chemotherapy has been tested and shown to improve therapeutic effects. To better understand cellular reactions to metronomic chemoendocrine therapy, we studied autophagy-related markers, beclin 1 and LC3, and apoptosis-related markers, TUNEL and M30, in pre- and post-treatment cancer tissues from a multicenter neoadjuvant trial, JBCRG-07, in which oral cyclophosphamide plus letrozole were administered to postmenopausal patients with HR-positive breast cancer. Changes in the levels of markers were compared with those following neoadjuvant endocrine therapy according to clinical response. Apoptosis, in addition to autophagy-related markers, increased following metronomic chemoendocrine therapy and such increases were associated with clinical response. By contrast, following endocrine therapy, the levels of apoptosis-related markers did not increase regardless of clinical response, whereas the levels of autophagy-related markers increased. Furthermore, levels of the apoptosis-related marker, M30, decreased in responders of endocrine therapy, suggesting that the induction of apoptosis by metronomic chemoendocrine therapy was involved in the improved clinical outcome compared with endocrine therapy. In conclusion, metronomic chemoendocrine therapy induced a different cellular reaction from that of endocrine therapy, including the induction of apoptosis, which is likely to contribute to improved efficacy compared with endocrine therapy alone. View Full-Text
Keywords: beclin 1; LC3; TUNEL; M30; autophagy; apoptosis; metronomic; chemoendocrine therapy; endocrine therapy beclin 1; LC3; TUNEL; M30; autophagy; apoptosis; metronomic; chemoendocrine therapy; endocrine therapy
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MDPI and ACS Style

Ueno, T.; Masuda, N.; Kamigaki, S.; Morimoto, T.; Saji, S.; Imoto, S.; Sasano, H.; Toi, M. Differential Involvement of Autophagy and Apoptosis in Response to Chemoendocrine and Endocrine Therapy in Breast Cancer: JBCRG-07TR. Int. J. Mol. Sci. 2019, 20, 984. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040984

AMA Style

Ueno T, Masuda N, Kamigaki S, Morimoto T, Saji S, Imoto S, Sasano H, Toi M. Differential Involvement of Autophagy and Apoptosis in Response to Chemoendocrine and Endocrine Therapy in Breast Cancer: JBCRG-07TR. International Journal of Molecular Sciences. 2019; 20(4):984. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040984

Chicago/Turabian Style

Ueno, Takayuki, Norikazu Masuda, Shunji Kamigaki, Takashi Morimoto, Shigehira Saji, Shigeru Imoto, Hironobu Sasano, and Masakazu Toi. 2019. "Differential Involvement of Autophagy and Apoptosis in Response to Chemoendocrine and Endocrine Therapy in Breast Cancer: JBCRG-07TR" International Journal of Molecular Sciences 20, no. 4: 984. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20040984

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