ArticleOncoTargets and therapy2018
Targeting DTL induces cell cycle arrest and senescence and suppresses cell growth and colony formation through TPX2 inhibition in human hepatocellular carcinoma cells.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 51 citations in OpenAlex.
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- Hepatocyte-specific angiotensinogen deficiency inhibits Western diet-induced liver steatosis with suppression of cell division in mice.Global translational medicine · 2025Article
- Rewired glycolysis by DTL accelerates oncometabolite L-lactate generation to promote breast cancer progression.Frontiers in oncology · 2025Article
- Deciphering molecular landscape of breast cancer progression and insights from functional genomics and therapeutic explorations followed by in vitro validation.Scientific reports · 2024Article
- DTL promotes the growth and migration of melanoma cells through the ERK/E2F1/BUB1 axis.Scientific reports · 2024Article
- Hypoxia-induced DTL promotes the proliferation, metastasis, and sorafenib resistance of hepatocellular carcinoma through ubiquitin-mediated degradation of SLTM and subsequent Notch pathway activation.Cell death & disease · 2024Article
- Osteopontin regulates the growth and invasion of liver cancer cells via DTL.Oncology letters · 2023Article
- Interaction gene set between osteoclasts and regulatory CD4Cancer science · 2023Article
- Pan-cancer analysis and experimental validation of DTL as a potential diagnosis, prognosis and immunotherapy biomarker.BMC cancer · 2023Article
- Circulating cell-free messenger RNA enables non-invasive pan-tumour monitoring of melanoma therapy independent of the mutational genotype.Clinical and translational medicine · 2022Article
- Identification and construction of a 13-gene risk model for prognosis prediction in hepatocellular carcinoma patients.Journal of clinical laboratory analysis · 2022Article
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- Overexpression of DTL enhances cell motility and promotes tumor metastasis in cervical adenocarcinoma by inducing RAC1-JNK-FOXO1 axis.Cell death & disease · 2021Article
- Bioinformatics analysis of lncRNA‑associated ceRNA network in melanoma.Journal of Cancer · 2021Article
- Identification of Key Biomarkers and Pathways in Small-Cell Lung Cancer Using Biological Analysis.BioMed research international · 2021Article
- MiR-490-5p Restrains Progression of Gastric cancer through DTL Repression.Gastroenterology research and practice · 2021Article
- Identification of genes associated with clinicopathological features of colorectal cancer.The Journal of international medical research · 2020Article
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Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) has an increasing incidence and high mortality. Surgical operation is not a comprehensive strategy for liver cancer. Moreover, tolerating systemic chemotherapy is difficult for patients with HCC because hepatic function is often impaired due to underlying cirrhosis. Therefore, a comprehensive strategy for cancer treatment should be developed. DTL (Cdc10-dependent transcript 2) is a critical regulator of cell cycle progression and genomic stability. In our previous study, the upregulation of DTL expression in aggressive HCC correlated positively with tumor grade and poor patient survival. We hypothesize that targeting DTL may provide a novel therapeutic strategy for liver cancer. DTL small interference RNAs were used to knock down DTL protein expression.
methodsA clonogenic assay, immunostaining, double thymidine block, imaging flow cytometry analysis, and a tumor spheroid formation assay were used to analyze the role of DTL in tumor cell growth, cell cycle progression, micronucleation, ploidy, and tumorigenicity.
resultsOur results demonstrated that targeting DTL reduced cell cycle regulators and chromosome segregation genes, resulting in increased cell micronucleation. DTL depletion inhibited liver cancer cell growth, increased senescence, and reduced tumorigenesis. DTL depletion resulted in the disruption of the mitotic proteins cyclin B, CDK1, securin, seprase, Aurora A, and Aurora B as well as the upregulation of the cell cycle arrest gene
conclusionOur study results indicate that DTL is a potential novel target gene for treating liver cancer through liver cancer cell senescence induction. Furthermore, our results provide insights into molecular mechanisms for targeting DTL in liver cancer cells. The results also indicate several other starting points for future preclinical and clinical studies on liver cancer treatment.
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