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

Zhao, S. J.; Fan, Suzhen; Shi, Yu; Ren, Hongyan; Hong, Hanqing; Gao, Xiang; Zhang, Min; Qin, Qiaohong; Li, Hongyu

doi:10.7150/jca.46556

Cited by 24 publications

(27 citation statements)

References 40 publications

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“…Similarly, propranolol also induces G0/G1/S phase arrest and apoptosis, leading to inhibition of proliferation in melanoma in vitro and in vivo by suppressing the AKT/MAPK signaling pathway [ 143 ]. Similar results were found in human ovarian cancer [ 144 ]. β2-AR blockage induces G1/S phase arrest and apoptosis in pancreatic cancer cells via Ras/Akt/NFκB pathway [ 145 ], or EFGR-Akt/ERK1/2 signaling pathway in colorectal cancer [ 146 ].…”

Section: Modulation Of the Tumor Microenvironment By Chronic Stressupporting

confidence: 88%

Highlighting the Potential for Chronic Stress to Minimize Therapeutic Responses to Radiotherapy through Increased Immunosuppression and Radiation Resistance

Chen

Singh

2020

Cancers

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Ionizing radiation has been used in the treatment of cancer for more than 100 years. While often very effective, there is still a great effort in place to improve the efficacy of radiation therapy for controlling the progression and recurrence of tumors. Recent research has revealed the close interaction between nerves and tumor progression, especially nerves of the autonomic nervous system that are activated by a variety of stressful stimuli including anxiety, pain, sleep loss or depression, each of which is likely to be increased in cancer patients. A growing literature now points to a negative effect of chronic stressful stimuli in tumor progression. In this review article, we present data on the potential for adrenergic stress to influence the efficacy of radiation and in particular, its potential to influence the anti-tumor immune response, and the frequency of an “abscopal effect” or the shrinkage of tumors which are outside an irradiated field. We conclude that chronic stress can be a major impediment to more effective radiation therapy through mechanisms involving immunosuppression and increased resistance to radiation-induced tumor cell death. Overall, these data highlight the potential value of stress reduction strategies to improve the outcome of radiation therapy. At the same time, objective biomarkers that can accurately and objectively reflect the degree of stress in patients over prolonged periods of time, and whether it is influencing immunosuppression and radiation resistance, are also critically needed.

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Section: Modulation Of the Tumor Microenvironment By Chronic Stressupporting

confidence: 88%

Highlighting the Potential for Chronic Stress to Minimize Therapeutic Responses to Radiotherapy through Increased Immunosuppression and Radiation Resistance

Chen

Singh

2020

Cancers

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“…In agreement, previous studies reported that propranolol significantly downregulates B cell lymphoma-2 and BCl-2 associated X protein, which may be related to the TLR4/NF-κB (p65) signal in isoproterenol-induced myocardial fibrosis in mice [ 179 , 180 , 181 ]. Recently, studies demonstrated that propranolol revealed significant suppression of p38 protein expression that primarily regulates cell proliferation, migration, cell differentiation, and BCL-2 family, inhibiting apoptosis [ 182 , 183 ]. In addition, BCl-2 is considered a tissue homeostasis indicator in vascular, heart, and neurodegenerative diseases [ 184 , 185 ].…”

Section: Resultsmentioning

confidence: 99%

Sustainable Release of Propranolol Hydrochloride Laden with Biconjugated-Ufasomes Chitosan Hydrogel Attenuates Cisplatin-Induced Sciatic Nerve Damage in In Vitro/In Vivo Evaluation

et al. 2022

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Peripheral nerve injuries significantly impact patients’ quality of life and poor functional recovery. Chitosan–ufasomes (CTS–UFAs) exhibit biomimetic features, making them a viable choice for developing novel transdermal delivery for neural repair. This study aimed to investigate the role of CTS–UFAs loaded with the propranolol HCl (PRO) as a model drug in enhancing sciatica in cisplatin-induced sciatic nerve damage in rats. Hence, PRO–UFAs were primed, embedding either span 20 or 60 together with oleic acid and cholesterol using a thin-film hydration process based on full factorial design (24). The influence of formulation factors on UFAs’ physicochemical characteristics and the optimum formulation selection were investigated using Design-Expert® software. Based on the optimal UFA formulation, PRO–CTS–UFAs were constructed and characterized using transmission electron microscopy, stability studies, and ex vivo permeation. In vivo trials on rats with a sciatic nerve injury tested the efficacy of PRO–CTS–UFA and PRO–UFA transdermal hydrogels, PRO solution, compared to normal rats. Additionally, oxidative stress and specific apoptotic biomarkers were assessed, supported by a sciatic nerve histopathological study. PRO–UFAs and PRO–CTS–UFAs disclosed entrapment efficiency of 82.72 ± 2.33% and 85.32 ± 2.65%, a particle size of 317.22 ± 6.43 and 336.12 ± 4.9 nm, ζ potential of −62.06 ± 0.07 and 65.24 ± 0.10 mV, and accumulatively released 70.95 ± 8.14% and 64.03 ± 1.9% PRO within 6 h, respectively. Moreover, PRO–CTS–UFAs significantly restored sciatic nerve structure, inhibited the cisplatin-dependent increase in peripheral myelin 22 gene expression and MDA levels, and further re-established sciatic nerve GSH and CAT content. Furthermore, they elicited MBP re-expression, BCL-2 mild expression, and inhibited TNF-α expression. Briefly, our findings proposed that CTS–UFAs are promising to enhance PRO transdermal delivery to manage sciatic nerve damage.

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“…MAPK/JNK is capable of regulating apoptosis after exposure to different stresses [ 313 ], and it can also regulate autophagy [ 314 , 315 ]. In prostate cancer cells, MAPK/JNK signaling induces autophagy as a protective mechanism against celecoxib-mediated apoptosis [ 316 ].…”

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Ashrafizadeh

Paskeh

Mirzaei

et al. 2022

J Exp Clin Cancer Res

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Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a “self-degradation” mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients. Graphical abstract

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

Cited by 24 publications

References 40 publications

Highlighting the Potential for Chronic Stress to Minimize Therapeutic Responses to Radiotherapy through Increased Immunosuppression and Radiation Resistance

Highlighting the Potential for Chronic Stress to Minimize Therapeutic Responses to Radiotherapy through Increased Immunosuppression and Radiation Resistance

Sustainable Release of Propranolol Hydrochloride Laden with Biconjugated-Ufasomes Chitosan Hydrogel Attenuates Cisplatin-Induced Sciatic Nerve Damage in In Vitro/In Vivo Evaluation

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

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