scholarly journals Mercury Chloride but Not Lead Acetate Causes Apoptotic Cell Death in Human Lung Fibroblast MRC5 Cells via Regulation of Cell Cycle Progression

2021 ◽  
Vol 22 (5) ◽  
pp. 2494
Author(s):  
Ji-Young Kim ◽  
Mi-Jin An ◽  
Geun-Seup Shin ◽  
Hyun-Min Lee ◽  
Mi Jin Kim ◽  
...  
Keyword(s):  
Heavy Metals ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Progression ◽  
Human Lung ◽  
Apoptotic Cell ◽  
Lung Fibroblast ◽  
Apoptotic Cell Death ◽  
Mercury Chloride ◽  
Human Lung Fibroblast

Heavy metals are important for various biological systems, but, in excess, they pose a serious risk to human health. Heavy metals are commonly used in consumer and industrial products. Despite the increasing evidence on the adverse effects of heavy metals, the detailed mechanisms underlying their action on lung cancer progression are still poorly understood. In the present study, we investigated whether heavy metals (mercury chloride and lead acetate) affect cell viability, cell cycle, and apoptotic cell death in human lung fibroblast MRC5 cells. The results showed that mercury chloride arrested the sub-G1 and G2/M phases by inducing cyclin B1 expression. In addition, the exposure to mercury chloride increased apoptosis through the activation of caspase-3. However, lead had no cytotoxic effects on human lung fibroblast MRC5 cells at low concentration. These findings demonstrated that mercury chloride affects the cytotoxicity of MRC5 cells by increasing cell cycle progression and apoptotic cell death.

scholarly journals Transcriptome Analysis Reveals HgCl2 Induces Apoptotic Cell Death in Human Lung Carcinoma H1299 Cells through Caspase-3-Independent Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 2006
Author(s):  
Mi Jin Kim ◽  
Jinhong Park ◽  
Jinho Kim ◽  
Ji-Young Kim ◽  
Mi-Jin An ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Transcriptome Analysis ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Expression Patterns ◽  
Nitrogen Compound ◽  
Apoptotic Cell Death ◽  
Mercury Chloride ◽  
Rna Seq

Mercury is one of the detrimental toxicants that can be found in the environment and exists naturally in different forms; inorganic and organic. Human exposure to inorganic mercury, such as mercury chloride, occurs through air pollution, absorption of food or water, and personal care products. This study aimed to investigate the effect of HgCl2 on cell viability, cell cycle, apoptotic pathway, and alters of the transcriptome profiles in human non-small cell lung cancer cells, H1299. Our data show that HgCl2 treatment causes inhibition of cell growth via cell cycle arrest at G0/G1- and S-phase. In addition, HgCl2 induces apoptotic cell death through the caspase-3-independent pathway. Comprehensive transcriptome analysis using RNA-seq indicated that cellular nitrogen compound metabolic process, cellular metabolism, and translation for biological processes-related gene sets were significantly up- and downregulated by HgCl2 treatment. Interestingly, comparative gene expression patterns by RNA-seq indicated that mitochondrial ribosomal proteins were markedly altered by low-dose of HgCl2 treatment. Altogether, these data show that HgCl2 induces apoptotic cell death through the dysfunction of mitochondria.

Presence of nanosilica (E551) in commercial food products: TNF-mediated oxidative stress and altered cell cycle progression in human lung fibroblast cells

2014 ◽  
Vol 30 (2) ◽  
pp. 89-100 ◽  
Author(s):  
Jegan Athinarayanan ◽  
Vaiyapuri Subbarayan Periasamy ◽  
Mohammed A. Alsaif ◽  
Abdulrahman A. Al-Warthan ◽  
Ali A. Alshatwi
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Human Lung ◽  
Food Products ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Cycle Progression ◽  
Human Lung Fibroblast ◽  
Altered Cell

scholarly journals RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Toshinori Ozaki ◽  
Akira Nakagawara ◽  
Hiroki Nagase
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Dna Damage Response ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Apoptotic Cell Death ◽  
Cycle Arrest ◽  
Damage Response

A proper DNA damage response (DDR), which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and/or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death such asp21WAF1,BAX, andPUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.

scholarly journals Antiproliferative activities of tricyclic amides derived from β-caryophyllene via the Ritter reaction against MDA-MB-231 breast cancer cells

2020 ◽  
Vol 11 (1) ◽  
pp. 118-124 ◽  
Author(s):  
XiXi Xu ◽  
Ariane Roseblade ◽  
Tristan Rawling ◽  
Alison T. Ung
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Apoptotic Cell ◽  
Ritter Reaction ◽  
Cycle Progression ◽  
The Ritter Reaction ◽  
Antiproliferative Activities

Tricyclic amides were successfully synthesised from β-caryophyllene via the Ritter reaction. Amides 3c and 6b inhibited proliferation of MDA-MB-231 cells. Compound 6b inhibited cell cycle progression and induced predominantly apoptotic cell death.

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