The biphosphinic paladacycle complex induces melanoma cell death through lysosomal–mitochondrial axis modulation and impaired autophagy

Gigli, Rafael Domingues.; Pereira, Gustavo José da Silva; Antunes, Fernanda; Bechara, Alexandre Henrique Silveira; Garcia, Daniel M.; Spindola, Daniel Gonsales; Jasiulionis, Miriam Galvonas; Caires, Antonio C. F.; Smaili, Soraya Soubhi; Bincoletto, Cláudia

doi:10.1016/j.ejmech.2015.11.008

Cited by 25 publications

(18 citation statements)

References 50 publications

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“…Some of these suggestions are based on the current literature and on previous studies published by our group demonstrating that combining different agents such as selumetinib and cytarabine with autophagy inhibitors (bafilomycin A1, chloroquine or 3-methyladenine) enhanced the activity of selumetinib and cytarabine against colorectal cancer cells 52 and leukemia cells 53 , respectively. Autophagy was also observed in melanoma cells under treatment with palladium complex drugs 54 , indicating the importance of investigating the relationship between autophagy and apoptosis during new drug development. Additionally, other studies demonstrated that inhibiting autophagy by chloroquine in combination with sorafenib in an in vitro model of glioblastoma 55 and in combination with temozolomide in melanoma patients augmented antitumor treatment efficacy 56 .…”

Section: Autophagy and Cancer Therapeuticsmentioning

confidence: 99%

Autophagy and intermittent fasting: the connection for cancer therapy?

Antunes

Erustes

Costa

et al. 2018

Clinics

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129

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Cancer is a leading cause of death worldwide, and its incidence is continually increasing. Although anticancer therapy has improved significantly, it still has limited efficacy for tumor eradication and is highly toxic to healthy cells. Thus, novel therapeutic strategies to improve chemotherapy, radiotherapy and targeted therapy are an important goal in cancer research. Macroautophagy (herein referred to as autophagy) is a conserved lysosomal degradation pathway for the intracellular recycling of macromolecules and clearance of damaged organelles and misfolded proteins to ensure cellular homeostasis. Dysfunctional autophagy contributes to many diseases, including cancer. Autophagy can suppress or promote tumors depending on the developmental stage and tumor type, and modulating autophagy for cancer treatment is an interesting therapeutic approach currently under intense investigation. Nutritional restriction is a promising protocol to modulate autophagy and enhance the efficacy of anticancer therapies while protecting normal cells. Here, the description and role of autophagy in tumorigenesis will be summarized. Moreover, the possibility of using fasting as an adjuvant therapy for cancer treatment, as well as the molecular mechanisms underlying this approach, will be presented.

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Section: Autophagy and Cancer Therapeuticsmentioning

confidence: 99%

Autophagy and intermittent fasting: the connection for cancer therapy?

Antunes

Erustes

Costa

et al. 2018

Clinics

Self Cite

129

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“…Autophagy modulation may be considered a new therapeutic strategy in treating patients with cancer [12][13][14][15]. The combination of autophagy inhibitors such as bafilomycin A1, chloroquine, or 3-methyladenine with standard agents has shown increased efficacy in treating tumor cells [16][17][18]. Notably, inhibition of autophagy demonstrated an increase response to radiotherapy in ovarian [19] and esophageal [20] cancer, likely due to enhanced oxidative stress and DNA damage during short-term fasting on cancer cells.…”

Section: Autophagymentioning

confidence: 99%

Energy and caloric restriction, and fasting and cancer: a narrative review

Ibrahim

Al‐Foheidi

Al‐Μansour

2020

Support Care Cancer

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Dietary interventions have a significant impact on body metabolism. The sensitivity of cancer cells to nutrient and energy deficiency is an evolving characteristic of cancer biology. Preclinical studies provided robust evidence that energy and caloric restrictions could hinder both cancer growth and progression, besides enhancing the efficacy of chemotherapy and radiation therapy. Moreover, several, albeit low-powered, clinical trials have demonstrated clinical benefits in cancer patients. Future research will inform and firmly establish the potential efficacy and safety of these dietary interventions. Here, we review the current evidence and ongoing research investigating the relationship between various dietary restriction approaches and cancer outcomes.

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“…Although autophagy has been considered as a mechanism for maintaining cell survival, an imbalance in cell metabolism when autophagic cellular consumption exceeds its capacity for synthesis may promote cell death . The process is morphologically distinct from apoptosis and is named ‘programmed type II cell death’.…”

Section: Autophagy and Cell Biologymentioning

confidence: 99%

Endoplasmic reticulum stress‐induced cell death in podocytes

Cheng

Chen

2017

Nephrology

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The authors explore how ER stress may induce cell death in podocytes, and how autophagy mediates to salvage the injuries caused by ER stress in the short term. ABSTRACT:Endoplasmic reticulum (ER) stress occurs in a variety of pathophysiological mechanisms, and there has been great interest in managing this pathway for the treatment of clinical diseases. Increased ER stress can block integrin-β1 glycosylation, decrease integrin-β1 protein expression and enhance cell death in podocytes. Autophagy is closely interconnected with ER stress to counteract the possible injurious effects related to the impairment of protein folding and is one of the intracellular protein degradation systems. Studies have shown that podocytes exhibit a high rate of autophagy to maintain as terminally differentiated cells. We have attempted to induce autophagy in podocytes with ER stress to increase the longevity of proteins and the degradation of damaged organelles. However, regardless of ER stress or autophagy that protects the cells at early stages, cells cannot adapt to this situation when the stress is already well established, and podocytes will undergo severe injury finally. In summary, ER stress may induce cell death in podocyte, and autophagy mediate to salvage the injuries caused by ER stress in the short term. It seems that adequate, but not excessive, autophagy is crucial to help maintain the cell viability of podocytes.

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The biphosphinic paladacycle complex induces melanoma cell death through lysosomal–mitochondrial axis modulation and impaired autophagy

Cited by 25 publications

References 50 publications

Autophagy and intermittent fasting: the connection for cancer therapy?

Autophagy and intermittent fasting: the connection for cancer therapy?

Energy and caloric restriction, and fasting and cancer: a narrative review

Endoplasmic reticulum stress‐induced cell death in podocytes

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