ArticleOncotarget2016
Ablation of human telomerase reverse transcriptase (hTERT) induces cellular senescence in gastric cancer through a galectin-3 dependent mechanism.
Article in Oncotarget, 2016. 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, 25 citations in OpenAlex.
- Pathways in the brain, heart and lung influenced by SARS-CoV-2 NSP6 and SARS-CoV-2 regulated miRNAs: an in silico study hinting cancer incidence.Cardio-oncology (London, England) · 2025Article
- Review
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- Spontaneous Preterm Birth: Elevated Galectin-3 and Telomere Shortening May Reflect a Common Pathway of Enhanced Inflammation and Senescence.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Galectins as pivotal components in oncogenesis and immune exclusion in human malignancies.Frontiers in immunology · 2023Review
- Knockdown of tankyrase 1 inhibits the progression of gastric adenocarcinoma via regulating human telomerase reverse transcriptase and telomeric repeat binding factor 1.Journal of gastrointestinal oncology · 2022Article
- Inhibition of galectins in cancer: Biological challenges for their clinical application.Frontiers in immunology · 2022Review
- Review
- Human chromosome 3p21.3 carries TERT transcriptional regulators in pancreatic cancer.Scientific reports · 2021Article
- Potential of Naturally Derived Compounds in Telomerase and Telomere Modulation in Skin Senescence and Aging.International journal of molecular sciences · 2021Review
- Combined CDK2 and CDK4/6 Inhibition Overcomes Palbociclib Resistance in Breast Cancer by Enhancing Senescence.Cancers · 2020Article
- Genomic and epigenomic EBF1 alterations modulate TERT expression in gastric cancer.The Journal of clinical investigation · 2020Article
- Non-classical role of Galectin-3 in cancer progression: translocation to nucleus by carbohydrate-recognition independent manner.BMB reports · 2020Review
- Sweetening the hallmarks of cancer: Galectins as multifunctional mediators of tumor progression.The Journal of experimental medicine · 2020Review
- Review
- A PDE1 inhibitor reduces adipogenesis in mice via regulation of lipolysis and adipogenic cell signaling.Experimental & molecular medicine · 2019Article
- Heat Shock Factor 1 Predicts Poor Prognosis of Gastric Cancer.Yonsei medical journal · 2018Article
- Galectin-3 supports stemness in ovarian cancer stem cells by activation of the Notch1 intracellular domain.Oncotarget · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human Telomerase Reverse Transcriptase (hTERT) gene encodes a rate-limiting catalytic subunit of telomerase that maintains genomic integrity. Suppression of hTERT expression could induce cellular senescence and is considered a potent approach for gastric cancer therapy. However, control of hTERT expression and function remains poorly understood in gastric cancer. In this study, we demonstrated that high expression levels of hTERT in malignant tissues are correlated with poor survival probability in gastric cancer patients. Knockdown of hTERT expression retarded cell proliferation and cellular senescence, which was confirmed by increased protein expression levels of p21cip1 and p27kip1, and decreased phosphorylation of Rb. In contrast, overexpression of hTERT increased cell proliferation and decreased cellular senescence. Remarkably, the down-regulation of hTERT expression was detected in lgals3-/- mouse embryo fibroblasts (MEFs). Knockdown of galectin-3 decreased the expression of hTERT in gastric cancer cells. Galectin-3 ablation-induced cellular senescence was rescued by concomitant overexpression of hTERT. hTERT ablation-induced cellular senescence and p21cip1 and p27kip1 expression was rescued by concomitant overexpression of galectin-3. The size of tumor burdens was increased in hTERT-overexpressed gastric cancer cells xenografted mice, whereas it was repressed by concomitant depletion of galectin-3. Additionally, we determined that the N-terminal domain of galectin-3 directly interacted with hTERT. The telomeric activity of hTERT was also decreased by galectin-3 ablation. Taken together, ablation of hTERT induces cellular senescence and inhibits the growth of gastric cancer cells, suggesting that it could be a potent target in gastric cancer therapy. We also propose that galectin-3 is an important regulator of hTERT expression and telomeric activity in gastric tumorigenesis.
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