ArticleNeuro-oncology2022
TRIM65 determines the fate of a novel subtype of pituitary neuroendocrine tumors via ubiquitination and degradation of TPIT.
Article in Neuro-oncology, 2022. 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, 31 citations in OpenAlex.
- Article
- Synergistic prognostic value of transcription factor multiplicity and Ki-67 in pituitary neuroendocrine tumour recurrence after endoscopic transsphenoidal surgery: a novel tiered molecular risk model.Frontiers in endocrinology · 2026Article
- Multidimensional tumor-blood profiling uncovers systemic lymphocyte-monocyte imbalance in pituitary neuroendocrine tumors.Signal transduction and targeted therapy · 2025Article
- The STUB1-TPIT axis regulates the secretion of adrenocorticotrophic hormone in cushing disease.Journal of translational medicine · 2025Article
- Aquaglyceroporin-7 ameliorates sorafenib resistance and immune evasion in hepatocellular carcinoma through inhibition of lipid accumulation.Cellular and molecular life sciences : CMLS · 2025Article
- TRIM65 regulates glucose metabolic reprogramming to promote glioma cell proliferation via ubiquitination and degradation of AMPK.NPJ precision oncology · 2025Article
- Cabergoline-induced NDFIP1 upregulation in pituitary neuroendocrine tumor cells activates mTOR signaling and contributes to cabergoline resistance.Journal of neuro-oncology · 2025Article
- Splicing diversity enhances the molecular classification of pituitary neuroendocrine tumors.Nature communications · 2025Article
- X-linked ubiquitin-specific peptidase 11 (USP11) increases susceptibility to Cushing's disease in women.Acta neuropathologica communications · 2025Article
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Knockdown of TRIM65 Inhibits Neoangiogenesis in Proliferative Diabetic Retinopathy by Regulating miR29a-3p.Current medicinal chemistry · 2025Article
- TRIM65 promotes renal cell carcinoma through ubiquitination and degradation of BTG3.Cell death & disease · 2024Article
- RNF126-mediated ubiquitination of FSP1 affects its subcellular localization and ferroptosis.Oncogene · 2024Article
- Single-cell transcriptomics reveal distinct immune-infiltrating phenotypes and macrophage-tumor interaction axes among different lineages of pituitary neuroendocrine tumors.Genome medicine · 2024Article
- Therapeutic potential of targeting Nrf2 by panobinostat in pituitary neuroendocrine tumors.Acta neuropathologica communications · 2024Article
- A systematic survey of LU domain-containing proteins reveals a novel human gene, LY6A, which encodes the candidate ortholog of mouse Ly-6A/Sca-1 and is aberrantly expressed in pituitary tumors.Frontiers of medicine · 2023Article
- DRD2 expression based onEndocrine · 2023Article
- Pathogenesis, clinical features, and treatment of plurihormonal pituitary adenoma.Frontiers in neuroscience · 2023Review
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundPituitary neuroendocrine tumors (PitNETs) are common intracranial tumors that are classified into seven histological subtypes, including lactotroph, somatotroph, corticotroph, thyrotroph, gonadotroph, null cell, and plurihormonal PitNETs. However, the molecular characteristics of these types of PitNETs are not completely clear.
methodsA total of 180 consecutive cases of PitNETs were collected to perform RNA sequencing. All subtypes of PitNETs were distinguished by unsupervised clustering analysis. We investigated the regulation of TPIT by TRIM65 and its effects on ACTH production and secretion in ACTH-secreting pituitary cell lines, as well as in murine models using biochemical analyses, confocal microscopy, and luciferase reporter assays.
resultsA novel subtype of PitNETs derived from TPIT lineage cells was identified as with normal TPIT transcription but with lowered protein expression. Furthermore, for the first time, TRIM65 was identified as the E3 ubiquitin ligase of TPIT. Depending on the RING domain, TRIM65 ubiquitinated and degraded the TPIT protein at multiple Lys sites. In addition, TRIM65-mediated ubiquitination of TPIT inhibited POMC transcription and ACTH production to determine the fate of the novel subtype of PitNETs in vitro and in vivo.
conclusionOur studies provided a novel classification of PitNETs and revealed that the TRIM65-TPIT complex controlled the fate of the novel subtype of PitNETs, which provides a potential therapy target for Cushing's disease.
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