HSP70 regulates cell proliferation and apoptosis in  actinomycin-D-treated lung cancer cells

Zhang, Kai; Zhai, Ruonan; Xue, Tong-Chun; Xu, Xiaoyan; Ren, Yanan; Ma, Mingze; Shi, Fengxian; Wang, Hang; Wang, Na; Zhou, Fang

doi:10.21037/tcr.2019.12.100

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…Cu has been found to be repressed in neurons with evidence of apoptosis; while Zn-SOD is known to bind and facilitate the production of significant amounts of endogenous peroxynitrite (ONOO−) [161][162][163]. Low concentrations of NO donors have been shown to inhibit neuroapoptosis induced by growth factor deprivation or TNF-α addition, potentially through the activation of the heat shock protein HSP70 or the inhibition of caspase-3 [164,165]. Dinitrosyl iron complexes (DNICs) at concentrations ranging from 5 to 10 μM are believed to suppress IL-1β-induced neuroapoptosis by promoting NO synthesis.…”

Section: Apoptosis and Nomentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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The regulation of cell death is a fundamental issue in cell biology and continues to be intensely investigated worldwide. The significance of research in this field persists because understanding the determinants of cell lifespan directly impacts the maintenance of multicellular organism homeostasis and, consequently, is crucial for addressing biomedical challenges associated with various diseases. It is recognized that the initiation of cell death can be prompted by both specific signals (such as cytokines or hormones) and nonspecific stimuli, including radiation, temperature increase, or oxidants. When these factors affect a cell, numerous signaling pathways are triggered in the cell, leading to neutralization of the effects of their negative effects or, in case of irreparable damage, to cell elimination. This removal of damaged cells occurs through apoptosis or programmed cell death, a highly regulated process. Numerous signaling molecules participate in orchestrating the apoptotic process, many of which also govern other essential functions within the organism. Physiological factors capable of triggering the apoptotic program in cells include nitric oxide (NO), which serves as one of the key signaling molecules regulating the functions of the cardiovascular, nervous, and immune systems of the organism. The unique chemical nature of NO, along with its numerous intracellular targets and physiologically active redox forms, raises questions about the specific mechanisms through which NO exerts its damaging effects on cells. Utilizing pharmacological preparations- such as sources (donors) of exogenous nitric oxide- represents an approach to investigating the initiation and execution of the apoptotic program in sensitive target cells. Furthermore, this approach holds promise as a direction for discovering new selective drugs.

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Section: Apoptosis and Nomentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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show abstract

“…Cu has been found to be repressed in neurons with evidence of apoptosis, while Zn-SOD is known to bind and facilitate the production of significant amounts of endogenous peroxynitrite (ONOO − ) [160][161][162]. Low concentrations of • NO donors have been shown to inhibit neuroapoptosis induced by growth factor deprivation or TNF-α addition, potentially through the activation of the heat shock protein HSP70 or the inhibition of caspase-3 [163,164]. Dinitrosyl iron complexes (DNICs) at concentrations ranging from 5 to 10 µM are believed to suppress IL-1β-induced neuroapoptosis by promoting • NO synthesis.…”

Section: Apoptosis and • Nomentioning

confidence: 99%

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Antioxidants

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Despite the significant progress in the fields of biology, physiology, molecular medicine, and pharmacology; the designation of the properties of nitrogen monoxide in the regulation of life-supporting functions of the organism; and numerous works devoted to this molecule, there are still many open questions in this field. It is widely accepted that nitric oxide (•NO) is a unique molecule that, despite its extremely simple structure, has a wide range of functions in the body, including the cardiovascular system, the central nervous system (CNS), reproduction, the endocrine system, respiration, digestion, etc. Here, we systematize the properties of •NO, contributing in conditions of physiological norms, as well as in various pathological processes, to the mechanisms of cytoprotection and cytodestruction. Current experimental and clinical studies are contradictory in describing the role of •NO in the pathogenesis of many diseases of the cardiovascular system and CNS. We describe the mechanisms of cytoprotective action of •NO associated with the regulation of the expression of antiapoptotic and chaperone proteins and the regulation of mitochondrial function. The most prominent mechanisms of cytodestruction—the initiation of nitrosative and oxidative stresses, the production of reactive oxygen and nitrogen species, and participation in apoptosis and mitosis. The role of •NO in the formation of endothelial and mitochondrial dysfunction is also considered. Moreover, we focus on the various ways of pharmacological modulation in the nitroxidergic system that allow for a decrease in the cytodestructive mechanisms of •NO and increase cytoprotective ones.

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Hyperthermia-mediated cell death via deregulation of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase signaling

Enomoto,

Fukasawa,

Yoshizaki

2024

Front. Cell Death

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Hyperthermia is a promising anticancer treatment that induces heat stress, thereby stimulating various signal transduction pathways to maintain cellular homeostasis. Mitogen-activated protein kinases (MAPKs) associate various extracellular stimuli with cytoplasmic and nuclear mediators through a three-tiered cascade of kinases, including MAPKs, MAP2Ks, and MAP3Ks. In mammals, three major groups of MAPKs have been characterized: extracellular signal-regulated protein kinases (ERK1/2), p38 MAPKs (α, β, γ, and δ), and c-Jun NH2-terminal kinases (JNK1/2/3). Each group of MAPKs is activated by heat and exhibits distinct biological functions. Recent studies have indicated that in hyperthermia, MAPK signaling pathways regulate cell survival and death in unique ways. This review offers a concise overview of the MAPK signaling pathway, specifically ERK and JNK, focusing on their relevance in cancer, interplay with heat shock proteins or phosphatases, and current understanding of the MAPK signaling pathway in hyperthermia.

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HSP70 regulates cell proliferation and apoptosis in actinomycin-D-treated lung cancer cells

Cited by 3 publications

References 22 publications

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection

Hyperthermia-mediated cell death via deregulation of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase signaling

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