ArticleiScience2022
L3MBTL2-mediated CGA transcriptional suppression promotes pancreatic cancer progression through modulating autophagy.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- L3MBTL2 as a novel therapeutic target for trigeminal neuralgia: evidence from integrated TWAS, multi-tissue MR, and experimental validation.The journal of headache and pain · 2025Article
- RHOD mediates ATG9A trafficking to promote autophagosome formation during autophagy in cancer.Autophagy · 2025Article
- Integrating bioinformatics and machine learning to discover sumoylation associated signatures in sepsis.Scientific reports · 2025Article
- Glycosylation-Related Genes and Prognostic Signatures in Diabetic Nephropathy.International journal of general medicine · 2025Article
- UBTF mediates activation of L3MBTL2 to suppress NISCH expression through histone H2AK119 monoubiquitination modification in breast cancer.Clinical & experimental metastasis · 2024Article
- Research advances of polycomb group proteins in regulating mammalian development.Frontiers in cell and developmental biology · 2024Review
- Augmenting L3MBTL2-induced condensates suppresses tumor growth in osteosarcoma.Science advances · 2023Article
- Cytoplasmic Expression of TP53INP2 Modulated by Demethylase FTO and Mutant NPM1 Promotes Autophagy in Leukemia Cells.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
L3MBTL2 is a crucial component of ncPRC1.6 and has been implicated in transcriptional repression and chromatin compaction. However, the repression mechanism of L3MBTL2 and its biological functions are largely undefined. Here, we found that L3MBTL2 plays a distinct oncogenic role in tumor development. We demonstrated that L3MBTL2 repressed downstream CGA through an H2AK119ub1-dependent mechanism. Importantly, the binding of the MGA/MAX heterodimer to the E-box on the CGA promoter enhanced the specific selective repression of CGA by L3MBTL2. CGA encodes the alpha subunit of glycoprotein hormones; however, we showed that CGA plays an individual tumor suppressor role in PDAC. Moreover, CGA-transcript1 (T1) was identified as the major transcript, and the tumor suppression function of CGA-T1 depends on its own glycosylation. Furthermore, glycosylated CGA-T1 inhibited PDAC, partly by repression of autophagy through multiple pathways, including PI3K/Akt/mTOR and TP53INP2 pathways. These findings reveal the important roles of L3MBTL2 and CGA in tumor development.
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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.