ArticleOncogene2006
hTERT: a novel endogenous inhibitor of the mitochondrial cell death pathway.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 citations in OpenAlex.
- Combining the Telomerase Inhibitor Imetelstat with the BCL-2 Inhibitor Venetoclax Enhances Apoptosis and Improves Survival in Acute Myeloid Leukemia Cellular and Animal Models.Journal of clinical medicine · 2026Article
- Article
- Accumulation of TERT in mitochondria exerts two opposing effects on apoptosis.FEBS open bio · 2023Article
- Review
- Many Functions of Telomerase Components: Certainties, Doubts, and Inconsistencies.International journal of molecular sciences · 2022Review
- The Role of Telomerase in Breast Cancer's Response to Therapy.International journal of molecular sciences · 2022Review
- Targeting telomerase reverse transcriptase with the covalent inhibitor NU-1 confers immunogenic radiation sensitization.Cell chemical biology · 2022Article
- Comprehensive Assessment ofCancers · 2020Article
- Non-canonical functions of Telomerase Reverse Transcriptase - Impact on redox homeostasis.Redox biology · 2020Review
- Human telomerase reverse transcriptase positively regulates mitophagy by inhibiting the processing and cytoplasmic release of mitochondrial PINK1.Cell death & disease · 2020Article
- Telomerase Reverse Transcriptase and p53 Regulate Mammalian Peripheral Nervous System and CNS Axon Regeneration Downstream of c-Myc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Exposure to environmental radionuclides associates with tissue-specific impacts on telomerase expression and telomere length.Scientific reports · 2019Article
- Telomerase Reverse Transcriptase Contains a BH3-Like Motif and Interacts with BCL-2 Family Members.Molecules and cells · 2018Article
- Epigenetic silencing of miR-296 and miR-512 ensures hTERT dependent apoptosis protection and telomere maintenance in basal-type breast cancer cells.Oncotarget · 2017Article
- Telomerase and drug resistance in cancer.Cellular and molecular life sciences : CMLS · 2017Review
- Association Between the Telomerase rs2736098_TT Genotype and a Lower Risk of Chronic Hepatitis B and Cirrhosis in Chinese Males.Clinical and translational gastroenterology · 2017Article
- Implications of telomeres and telomerase in endometrial pathology.Human reproduction update · 2017Review
- Hsp90-binding immunophilin FKBP51 forms complexes with hTERT enhancing telomerase activity.Molecular oncology · 2016Article
- hTERT promotes cell adhesion and migration independent of telomerase activity.Scientific reports · 2016Article
- MST-312 induces G2/M cell cycle arrest and apoptosis in APL cells through inhibition of telomerase activity and suppression of NF-κB pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
hTERT is the catalytic subunit of the telomerase and is hence required for telomerase maintenance activity and cancer cell immortalization. Here, we show that acute hTERT depletion has no adverse effects on the viability or proliferation of cervical and colon carcinoma cell lines, as evaluated within 72 h after transfection with hTERT-specific small interfering RNAs (siRNAs). Within the same time frame, hTERT depletion facilitated the induction of apoptotic cell death by cisplatin, etoposide, mitomycin C and reactive oxygen species, yet failed to sensitize cells to death induction via the CD95 death receptor. Experiments performed with p53 knockout cells or chemical p53 inhibitors revealed that p53 was not involved in the chemosensitizing effect of hTERT knockdown. However, the proapoptotic Bcl-2 family protein Bax was involved in cell death induction by hTERT siRNAs. Depletion of hTERT facilitated the conformational activation of Bax induced by genotoxic agents. Moreover, Bax knockout abolished the chemosensitizing effect of hTERT siRNAs. Inhibition of mitochondrial membrane permeabilization by overexpression of Bcl-2 or expression of the cytomegalovirus-encoded protein vMIA (viral mitochondrial inhibitor of apoptosis), which acts as a specific Bax inhibitor, prevented the induction of cell death by the combination of hTERT depletion and chemotherapeutic agents. Altogether, our data indicate that hTERT inhibition may constitute a promising strategy for facilitating the induction of the mitochondrial pathway of apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.