ArticlePloS one2011
Twisted epithelial-to-mesenchymal transition promotes progression of surviving bladder cancer T24 cells with hTERT-dysfunction.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.Medical oncology (Northwood, London, England) · 2025Review
- Effects of p53 and ATRX inhibition on telomeric recombination in aging fibroblasts.Frontiers in oncology · 2024Article
- The neuronal protein Neuroligin 1 promotes colorectal cancer progression by modulating the APC/β-catenin pathway.Journal of experimental & clinical cancer research : CR · 2022Article
- The telomere maintenance mechanism spectrum and its dynamics in gliomas.Genome medicine · 2022Article
- Biomarker LEPRE1 induces pelitinib-specific drug responsiveness by regulating ABCG2 expression and tumor transition states in human leukemia and lung cancer.Scientific reports · 2022Article
- SLX4IP N-terminus dictates telomeric localization in ALT-like castration-resistant prostate cancer cell lines.The Prostate · 2021Article
- Alternative lengthening of telomeres is mechanistically linked to potential therapeutic vulnerability in the stem-like subtype of gastric cancer.Clinical and translational medicine · 2021Article
- SLX4IP Promotes Telomere Maintenance in Androgen Receptor-Independent Castration-Resistant Prostate Cancer through ALT-like Telomeric PML Localization.Molecular cancer research : MCR · 2021Article
- Review
- Combination Therapy with Nanomicellar-Curcumin and Temozolomide for In Vitro Therapy of Glioblastoma Multiforme via Wnt Signaling Pathways.Journal of molecular neuroscience : MN · 2020Article
- "Mitotic Slippage" and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres.International journal of molecular sciences · 2020Article
- Review
- Stem cells, immortality, and the evolution of metastatic properties in breast cancer: telomere maintenance mechanisms and metastatic evolution.Journal of cancer metastasis and treatment · 2019Article
- Telomere Length Maintenance in Cancer: At the Crossroad between Telomerase and Alternative Lengthening of Telomeres (ALT).International journal of molecular sciences · 2018Review
- Expanding the chemotherapeutic potential of an established nucleoside analog with selective targeting of telomerase.Molecular & cellular oncology · 2018Article
- WNT signaling in glioblastoma and therapeutic opportunities.Laboratory investigation; a journal of technical methods and pathology · 2016Review
- Regulatory Snapshots: integrative mining of regulatory modules from expression time series and regulatory networks.PloS one · 2012Article
- Telomerase-independent paths to immortality in predictable cancer subtypes.Journal of Cancer · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman cancer cells maintain telomeres to protect cells from senescence through telomerase activity (TA) or alternative lengthening of telomeres (ALT) in different cell types. Moreover, cellular senescence can be bypassed by Epithelial-to-mesenchymal transition (EMT) during cancer progression in diverse solid tumors. However, it has not been elucidated the characteristics of telomere maintenance and progression ability after long-term culture in bladder cancer T24 cells with hTERT dysfunction. METHODOLOGY/PRINCIPAL
findingsIn this study, by using a dominant negative mutant human telomerase reverse transcriptase (hTERT) vector to inhibit TA in bladder cancer T24 cells, we observed the appearance of long phenotype of telomere length and the ALT-associated PML body (APB) complex after the 27(th) passage, indicating the occurrence of ALT-like pathway in surviving T24/DN868A cells with telomerase inhibition. Meanwhile, telomerase inhibition resulted in significant EMT as shown by change in cellular morphology concomitant with variation of EMT markers. Consistently, the surviving T24/DN868A cells showed increased progression ability in vitro and in vivo. In addition, we found Twist was activated to mediate EMT in surviving T24/DN868A samples. CONCLUSIONS/SIGNIFICANCE: Taken together, our findings indicate that bladder cancer T24 cells may undergo the telomerase-to-ALT-like conversion and promote cancer progression at advanced stages through promoting EMT, thus providing novel possible insight into the mechanism of resistance to telomerase inhibitors in cancer treatment.
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