Risk of wild fungi treatment failure: Phallus impudicus-induced telomere damage triggers p21/p53 and p16-dependent cell cycle arrest and may contribute to male fertility reduction in vitro

Sołek, Przemysław; Shemedyuk, Nataliya; Shemedyuk, Anastasiya; Dudzińska, Ewa; Koziorowski, Marek

doi:10.1016/j.ecoenv.2020.111782

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…Our data revealed that nicotine exerts anti-proliferative effect because of p53-dependent cell cycle arrest in the G2/M phase mediated by p16 in hPDLSCs, indicating that nicotine dramatically induces an increase in the ratio of cells in the G2/M phase and inhibited the cell division, which lead to the decrease of G0/G1 cells ratio, a quiescent phase of the cell cycle. 26 Interestingly, except for the regulation of cell cycle, it is widely known that p53 and p16 are also typical markers of cellular senescence. Hence, the upregulation of p53 and p16 by induction of nicotine may also suggest that nicotine could influence the pre-senescence of hPDLSCs, which still needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Nicotine destructs dental stem cell-based periodontal tissue regeneration

Jiang

Yang

Jia

et al. 2024

Journal of Dental Sciences

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Section: Discussionmentioning

confidence: 99%

Nicotine destructs dental stem cell-based periodontal tissue regeneration

Jiang

Yang

Jia

et al. 2024

Journal of Dental Sciences

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“…Knockdown of TRF2 in healthy T cells increased in telomeric DNA damage and T cell apoptosis. In contrast, overexpression of TRF2 in HCV T cells alleviated telomeric DNA damage and T cell apoptosis [ 38 ]. Our present research found that knockdown of TRF2 significantly exacerbated apoptosis in gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of TRF2 Leads to Ferroptosis, Autophagic Death, and Apoptosis by Causing Telomere Dysfunction

Yang

Nie

Zhu

et al. 2023

Oxidative Medicine and Cellular Longevity

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Background. Gastric cancer (GC) is an aggressive malignancy with a high mortality rate and poor prognosis. Telomeric repeat-binding factor 2 (TRF2) is a critical telomere protection protein. Emerging evidence indicates that TRF2 may be an essential treatment option for GC; however, the exact mechanism remains largely unknown. Objective. We aimed to explore the role of TRF2 in GC cells. The function and molecular mechanisms of TRF2 in the pathogenesis of GC were mainly discussed in this study. Methods. Relevant data from GEPIA and TCGA databases regarding TRF2 gene expression and its prognostic significance in GC samples were analyzed. Analysis of 53BP1 foci at telomeres by immunofluorescence, metaphase spreads, and telomere-specific FISH analysis was carried out to explore telomere damage and dysfunction after TRF2 depletion. CCK8 cell proliferation, trypan blue staining, and colony formation assay were performed to evaluate cell survival. Apoptosis and cell migration were determined with flow cytometry and scratch-wound healing assay, respectively. qRT-PCR and Western blotting were carried out to analyze the mRNA and protein expression levels after TRF2 depletion on apoptosis, autophagic death, and ferroptosis. Results. By searching with GEPIA and TCGA databases, the results showed that the expression levels of TRF2 were obviously elevated in the samples of GC patients, which was associated with adverse prognosis. Knockdown of TRF2 suppressed the cell growth, proliferation, and migration in GC cells, causing significant telomere dysfunction. Apoptosis, autophagic death, and ferroptosis were also triggered in this process. The pretreatment of chloroquine (autophagy inhibitor) and ferrostatin-1 (ferroptosis inhibitor) improved the survival phenotypes of GC cells. Conclusion. Our data suggest that TRF2 depletion can inhibit cell growth, proliferation, and migration through the combined action of ferroptosis, autophagic death, and apoptosis in GC cells. The results indicate that TRF2 might be used as a potential target to develop therapeutic strategies for treating GC.

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“…In human normal cells, the p53 gene plays an important role in avoiding the accumulation of damaged DNA, maintaining genomic stability, and regulating cell differentiation and senescence by inducing cell cycle arrest and promoting cell apoptosis and DNA repair 33–37 . p53‐related target genes include p21, MDM2, CD95, fas, Bax, HER2, and PCNA.…”

Section: Discussionmentioning

confidence: 99%

C2orf40 inhibits hepatocellular carcinoma through interaction with UBR5

Qin

et al. 2021

J of Gastro and Hepatol

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Background and Aim Hepatocellular carcinoma (HCC) urgently needs a marker for early diagnosis and targeted treatment. C2orf40 has been identified as a tumor suppressor gene in many cancers. However, the precise role and regulatory mechanism by C2orf40 contribute to HCC remain elusive and merit exploration. Methods Reverse‐transcription PCR, quantitative real‐time PCR, and methylation‐specific PCR were used to detect expression and methylation of C2orf40 in HCC cell lines or tissues. The effects of C2orf40 in liver cancer cells were examined via colony formation, CCK8, transwell, and flow cytometric assays. The effect of C2orf40 on tumorigenesis in vivo was determined by xenografts and immunohistochemical analysis. Western blot, indirect immunofluorescence, Co‐IP, and cycloheximide (CHX) were used to further investigate the potential mechanism of C2orf40. Results The down‐regulation of C2orf40 in hepatocellular cancer tissue samples is often related to the degree of methylation of its promoter CpG. The recovery of C2orf40 expression in HCC cell lines can induce G0/G1 phase arrest and apoptosis and also inhibit cell migration and invasion by reversing the epithelial–mesenchymal transition (EMT) process, both in vivo and in vitro. In addition, C2orf40 can increase the expression of p21 through interaction with UBR5. Conclusions Low expression levels of C2orf40 are related to the hypermethylation of its promoter. C2orf40 can inhibit HCC through UBR5‐dependent or p53‐independent mechanisms. C2orf40 may be a diagnostic biomarker and a potential therapeutic target in HCC.

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Risk of wild fungi treatment failure: Phallus impudicus-induced telomere damage triggers p21/p53 and p16-dependent cell cycle arrest and may contribute to male fertility reduction in vitro

Cited by 5 publications

References 38 publications

Nicotine destructs dental stem cell-based periodontal tissue regeneration

Nicotine destructs dental stem cell-based periodontal tissue regeneration

Inhibition of TRF2 Leads to Ferroptosis, Autophagic Death, and Apoptosis by Causing Telomere Dysfunction

C2orf40 inhibits hepatocellular carcinoma through interaction with UBR5

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