Propranolol induced apoptosis and autophagy  via  the ROS/JNK signaling pathway in Human Ovarian Cancer

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Abstract

Propranolol has a significant anti-cancer effect towards various cancers. Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase therefore leading to apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.

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Autophagy and multidrug resistance in cancer

Ying-Jie Li, Yu-He Lei, Nan Yao … (2017)

Multidrug resistance (MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence. Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells.

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Surgical stress promotes tumor growth in ovarian carcinoma.

Guillermo Armaiz-Pena, P J Halder, N Jennings … (2009)

Surgical stress has been suggested to facilitate the growth of preexisting micrometastases as well as small residual tumor postoperatively. The purpose of this study was to examine the effects of surgical stress on ovarian cancer growth and to determine underlying mechanisms responsible for increased growth. To mimic the effects of surgery, we did a laparotomy or mastectomy under isoflurane inhalation on athymic nude mice 4 days after i.p. tumor cell injection. Propranolol infusion via Alzet pumps was used to block the influence of sympathetic nervous system activation by surgical stress. In both HeyA8 and SKOV3ip1 models, the mice in the laparotomy and mastectomy groups had significantly greater tumor weight (P < 0.05) and nodules (P < 0.05) compared with anesthesia only controls. There was no increase in tumor weight following surgery in the beta-adrenergic receptor-negative RMG-II model. Propranolol completely blocked the effects of surgical stress on tumor growth, indicating a critical role for beta-adrenergic receptor signaling in mediating the effects of surgical stress on tumor growth. In the HeyA8 and SKOV3ip1 models, surgery significantly increased microvessel density (CD31) and vascular endothelial growth factor expression, which were blocked by propranolol treatment. These results indicate that surgical stress could enhance tumor growth and angiogenesis, and beta-blockade might be effective in preventing such effects.

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Screening for Ovarian Cancer

David Grossman, Susan Curry, Douglas Owens … (2018)

With approximately 14 000 deaths per year, ovarian cancer is the fifth most common cause of cancer death among US women and the leading cause of death from gynecologic cancer. More than 95% of ovarian cancer deaths occur among women 45 years and older.

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Author and article information

Journal

Journal ID (nlm-ta): J Cancer

Journal ID (iso-abbrev): J Cancer

Journal ID (publisher-id): jca

Title: Journal of Cancer

Publisher: Ivyspring International Publisher (Sydney )

ISSN (Electronic): 1837-9664

Publication date Collection: 2020

Publication date (Electronic): 10 August 2020

Volume: 11

Issue: 20

Pages: 5900-5910

Affiliations

[1 ]Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Zhengzhou, 450000, P.R.China.

[2 ]Zhengzhou Key Laboratory of Gynecological Oncology, 450052 Zhengzhou, China.

Author notes

✉ Corresponding author: Hongyu Li (Professor, Director), Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Zhengzhou, 450000, P.R.China. E-mail: hongyuli163@ 123456163.com .

Competing Interests: The authors have declared that no competing interest exists.

Article

Publisher ID: jcav11p5900

DOI: 10.7150/jca.46556

PMC ID: 7477428

PubMed ID: 32922532

SO-VID: 40f4a001-6f5b-48de-9bf6-98c0377ce055

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer

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Karger: Oncology

Most cited references 26

Autophagy and multidrug resistance in cancer

Surgical stress promotes tumor growth in ovarian carcinoma.

Screening for Ovarian Cancer

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