ArticleCell & bioscience2021
TRIM28 inhibits alternative lengthening of telomere phenotypes by protecting SETDB1 from degradation.
Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- TRIM28 Increases RFC4 Protein Expression to Promote Triple-Negative Breast Cancer Progression.MedComm · 2026Article
- ZNF184 negatively regulates HR repair and predicts poor prognosis in acute lymphoblastic leukemia.Nucleic acids research · 2026Article
- Orphan nuclear receptors recruit TRIM28 to promote telomeric H3K9me3 for the ALT pathway.The EMBO journal · 2026Article
- Local heterochromatin enrichment promotes telomere clustering and PML nuclear body assembly at telomeres.Cell reports · 2026Article
- Shugoshin 2A stabilizes heterochromatin complexes to suppress the 2-cell-like state in embryonic stem cells.Stem cell reports · 2026Article
- Interaction of AURKA with TRIM28 revives dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis.Cancer cell international · 2025Article
- Identification of alternative lengthening of telomeres-related genes prognosis model in hepatocellular carcinoma.BMC cancer · 2024Article
- A First-in-Class High-Throughput Screen to Discover Modulators of the Alternative Lengthening of Telomeres (ALT) Pathway.ACS pharmacology & translational science · 2024Article
- How calorie restriction slows aging: an epigenetic perspective.Journal of molecular medicine (Berlin, Germany) · 2024Review
- The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease.Epigenetics & chromatin · 2023Review
- The Altered Functions of Shelterin Components in ALT Cells.International journal of molecular sciences · 2023Review
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundAbout 10-15% of tumor cells extend telomeres through the alternative lengthening of telomeres (ALT) mechanism, which is a recombination-dependent replication pathway. It is generally believed that ALT cells are related to the chromatin modification of telomeres. However, the mechanism of ALT needs to be further explored.
resultsHere we found that TRIM28/KAP1 is preferentially located on the telomeres of ALT cells and interacts with telomeric shelterin/telosome complex. Knocking down TRIM28 in ALT cells delayed cell growth, decreased the level of C-circle which is one kind of extrachromosomal circular telomeric DNA, increased the frequency of ALT-associated promyelocytic leukemia bodies (APBs), led to telomere prolongation and increased the telomere sister chromatid exchange in ALT cells. Mechanistically, TRIM28 protects telomere histone methyltransferase SETDB1 from degradation, thus maintaining the H3K9me3 heterochromatin state of telomere DNA.
conclusionsOur work provides a model that TRIM28 inhibits alternative lengthening of telomere phenotypes by protecting SETDB1 from degradation. In general, our results reveal the mechanism of telomere heterochromatin maintenance and its effect on ALT, and TRIM28 may serve as a target for the treatment of ALT tumor cells.
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