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Cited by 8Trace Elements in HealthCell death mechanisms and regulationHeavy Metal Exposure and Toxicity

Low Zinc Environment Induces Stress Signaling, Senescence and Mixed Cell Death Modalities in Colon Cancer Cells

Rudolf, Emil, Rudolf, Kamil·2015·Apoptosis
DOI 10.1007/s10495-015-1182-5
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Abstract

Currently it is not clear what type of the final cellular response (i.e. cell death modality or senescence) is induced upon chronic intracellular zinc depletion in colon cancer cells. To address this question, isogenic colon cancer lines SW480 and SW620 exposed to low zinc environment were studied over the period of 6 weeks. Low zinc environment reduced total as well as free intracellular zinc content in both cell lines. Decreased intracellular zinc content resulted in changes in cellular proliferation, cell cycle distribution and activation of stress signaling. In addition, colonocytes with low zinc content displayed increased levels of oxidative stress, changes in mitochondrial activity but in the absence of significant DNA damage. Towards the end of treatment (4th-6th week), exposed cells started to change morphologically, and typical markers of senescence as well as cell death appeared. Of two examined colon cancer cell lines, SW480 cells proved to activate predominantly senescent phenotype, with frequent form of demise being necrosis and mixed cell death modality but not apoptosis. Conversely, SW620 cells activated mostly cell death, with relatively equal distribution of apoptosis and mixed types, while senescent phenotypes and necrosis were present only in a small fraction of cell populations. Addition of zinc at the beginning of 4th week of treatment significantly suppressed cell death phenotypes in both cell lines but had no significant effect on senescence. In conclusion, presented results demonstrate variability of responses to chronic zinc depletion in colon cancer as modeled in vitro.

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Crossref · 10.1007/s10495-015-1182-5

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  • The structural and functional roles of zinc, selenium, magnesium, copper, and manganese are crucial for antioxidant defence.

    “Concerning the latter, the structural and functional roles of a few minerals such as zinc (Zn), selenium (Se), magnesium (Mg) copper (Cu) and manganese (Mn) is crucial (Table 5) [409,410,411,412,413,414,415,416,417,418,419,420].”

    From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [409]

  • In a colon cancer cell line and dermal fibroblasts, zinc dysregulation promotes cellular senescence by activating stress response and pro-apoptosis pathways.

    “For instance, in a colon cancer cell line [409] and dermal fibroblasts [410], Zn dysregulation promoted cellular senescence activating stress response and pro-apoptosis pathways.”

    From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [409]

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Authors
Rudolf, E., & Rudolf, K.
Affiliations
Charles University (CZ)
Corresponding author
Rudolf, Emil
ORCID
Venue
Apoptosis
Publisher
Springer Science and Business Media LLC
Published
2015-10-07
Volume
20
Issue
12
Pages
1651-1665
ISSN
  • 1360-8185 (ISSN-L)
  • 1573-675X
DOI
10.1007/s10495-015-1182-5
OpenAlex
W2268712294
Cited by
8
References
50
Citations by year
2023: 2 · 2022: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2016: 1
FWCI
0.64
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • APOPTOSIS (publishedVersion)
  • PubMed (publishedVersion)
Funders
PRVOUK (P37/01)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
Keywords
zinc depletion, intracellular zinc, colon cancer, cellular senescence, necrosis, oxidative stress, mitochondrial activity, stress signaling, cell cycle, zinc supplementation, SW480 cells, SW620 cells
MeSH terms
Cell Cycle, Colonic Neoplasms, DNA Damage, Humans, Necrosis, Zinc, Signal Transduction, Cellular Senescence, Cell Death, Apoptosis, Oxidative Stress, Cell Line, Tumor, Cell Proliferation

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