Bystander Me45 Melanoma Cells Increase Damaging Effect in <scp>UVC</scp>‐irradiated Cells

Krzywon, Aleksandra; Wideł, Maria

doi:10.1111/php.13080

Cited by 4 publications

(2 citation statements)

References 45 publications

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“…Similar phenomenon can be observed in UV radiation as well (Eftekhari and Fardid, 2019). Krzywon and Widel (2019) found that viability of non-irradiated cells would be reduced when coincubated with irradiated cells. Induction of cell-cycle arrest at the G2/M transition was observed in nonirradiated cells treated with conditioned medium from UVCirradiated A375 human melanoma cells (Ghosh et al, 2013).…”

Section: Introductionsupporting

confidence: 77%

Exosomal MiR-769-5p Exacerbates Ultraviolet-Induced Bystander Effect by Targeting TGFBR1

Tao

et al. 2020

Front. Physiol.

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Exosomal microRNAs have been investigated in bystander effect, but it is unclear whether microRNA works in ultraviolet radiation–induced bystander effects (UV-RIBEs) and what the underlying mechanism could be. Exosomes from ultraviolet (UV)–irradiated human skin fibroblasts (HSFs) were isolated and transferred to normal HSFs, followed by the detection of proliferation rate, oxidative damage level, and apoptosis rate. Exosomal miRNAs were evaluated and screened with miRNA sequencing and quantitative reverse transcriptase–polymerase chain reaction method. MiRNA shuttle and bystander photodamage reactions were observed after transfection of miR-769-5p. MiR-769-5p targeting gene transforming growth factor-β1 (TGFBR1), and TGFBR1 mRNA 3′-untranslated region (UTR) was assessed and identified by Western blotting and dual-luciferase reporter assay. Bystander effects were induced after being treated with isolated exosomes from UV-irradiated HSFs. Exosomal miR-769-5p expression was significantly upregulated. Human skin fibroblasts showed lower proliferation, increasing oxidative damage, and faster occurrence of apoptosis after transfection. Exosome-mediated transfer of miR-769-5p was observed. Upregulation of miR-769-5p induced bystander effects, whereas downregulation of miR-769-5p can suppress UV-RIBEs. In addition, miR-769-5p was found to downregulate TGFBR1 gene expression by directly targeting its 3′-UTR. Our results demonstrate that exosome-mediated miR-769-5p transfer could function as an intercellular messenger and exacerbate UV-RIBEs. MiR-769-5p inhibits the expression of TGFBR1 by targeting TGFBR1 mRNA 3′-UTR.

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Section: Introductionsupporting

confidence: 77%

Exosomal MiR-769-5p Exacerbates Ultraviolet-Induced Bystander Effect by Targeting TGFBR1

Tao

et al. 2020

Front. Physiol.

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“…In further studies, potential p42/44 ERKs-, AKT-and p38-mediated phosphorylation of ERα in UVC-treated cells is to be investigated. UV irradiation has been indicated to stimulate the bystander effect (48), with corresponding events such as apoptosis, premature senescence, single and double DNA strand breaks, and reduced clonogenic survival described in bystander cells (49).…”

Section: Discussionmentioning

confidence: 99%

Irreversible inhibition of estrogen receptor α signaling and the emergence of hormonal resistance in MCF7 breast cancer cells induced by DNA damage agents

Scherbakov,

Sorokin,

Razuvaeva

et al. 2024

Biomed Rep

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Combining chemotherapy and hormone therapy is a prevalent approach in breast cancer treatment. While the cytotoxic impact of numerous chemotherapy drugs stems from DNA damage, the exact role of these DNA alterations in modulating estrogen receptor α (ERα) machinery remains elusive. The present study aimed to analyze the impact of DNA damage agents on ERα signaling in breast cancer cells and assess the signaling pathways mediating the influence of DNA damage drugs on the ERα machinery. Cell viability was assessed using the MTT method, while the expression of signaling proteins was analyzed by immunoblotting. ERα activity in the cells treated with various drugs (17β-estradiol, tamoxifen, 5-fluorouracil) was assessed through reporter gene assays. In vitro experiments were conducted on MCF7 breast cancer cells subjected to varying durations of 5-fluorouracil (5-FU) treatment. Two distinct cell responses to 5-FU were identified based on the duration of the treatment. A singular dose of 5-FU induces pronounced DNA fragmentation, temporally suppressing ERα signaling while concurrently activating AKT phosphorylation. This suppression reverses upon 5-FU withdrawal, restoring normalcy within ten days. However, chronic 5-FU treatment led to the emergence of 5-FU-resistant cells with irreversible alterations in ERα signaling, resulting in partial hormonal resistance. These changes mirror those observed in cells subjected to UV-induced DNA damage, underscoring the pivotal role of DNA damage in shaping estrogen signaling alterations in breast cancer cells. In summary, the results of the present study suggested that the administration of DNA damage agents to cancer cells can trigger irreversible suppression of estrogen signaling, fostering the development of partial hormonal resistance. This outcome may ultimately impede the efficacy of combined or subsequent chemo-and hormone therapy strategies.

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Cytogenetic effects in mixed culture of blood cells from patients with chronic lymphocytic leukemia with blood lymphocytes of healthy individuals

Pilinska¹,

Shemetun²,

Talan³

et al. 2020

Dopov. Nac. akad. nauk Ukr.

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Одним із проявів універсального феномену bystander response як відповіді нормальних клітин (свідків) на генотоксичний стрес, індукований клітинами-мішенями, є нещодавно відкритий прямий і зворотний пухлино-індукований ефект свідка (tumor-induced bystander effect (TIBE))-результат взаємодії між здоровими та злоякісними клітинами [1, 2]. Здатність до індукції ТІВЕ встановлено, зокрема, для клітин меланоми та аденокарциноми легенів за умов їх сумісного культивування з нормальними клітинами з різних тканин люди

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Bystander Me45 Melanoma Cells Increase Damaging Effect in UVC‐irradiated Cells

Cited by 4 publications

References 45 publications

Exosomal MiR-769-5p Exacerbates Ultraviolet-Induced Bystander Effect by Targeting TGFBR1

Exosomal MiR-769-5p Exacerbates Ultraviolet-Induced Bystander Effect by Targeting TGFBR1

Irreversible inhibition of estrogen receptor α signaling and the emergence of hormonal resistance in MCF7 breast cancer cells induced by DNA damage agents

Cytogenetic effects in mixed culture of blood cells from patients with chronic lymphocytic leukemia with blood lymphocytes of healthy individuals

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