ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
TBC1D22B Regulates ER-to-Golgi Trafficking via RAB1B Inactivation and Promotes Oncogenic Programs in Breast Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Alternative splicing events show high prognostic values and indicate potential core genes in acute myeloid leukemia.Clinical and experimental medicine · 2026Article
- TBC1D22B Regulates ER-to-Golgi Trafficking via RAB1B Inactivation and Promotes Oncogenic Programs in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
TBC1D22B is a GTPase-activating protein (GAP) associated with poor prognosis in breast cancer (BC). Using complementary proximity-labeling and co-immunoprecipitation proteomics, the TBC1D22B interactome in BC cells is defined, revealing strong enrichment in components of the ER-to-Golgi trafficking machinery, endosomal transport, and adhesion-related pathways. Functional assays, using the Retention Using Selective Hooks (RUSH) system, demonstrate that TBC1D22B inhibits ER-to-Golgi transport in a GAP-dependent manner. Mechanistic studies identify RAB1B as a direct target of TBC1D22B, and RAB1B silencing phenocopies the trafficking defects caused by TBC1D22B overexpression. In 3D culture, TBC1D22B promotes spheroid growth in a manner dependent on its GAP activity and not replicated by its paralog TBC1D22A. Transcriptomic profiling reveals that TBC1D22B overexpression triggers repression of a core module of extracellular matrix and adhesion-related genes, consistent with altered secretory activity. Importantly, this transcriptional program is also evident in primary Luminal BC with high TBC1D22B expression, highlighting a conserved and functionally relevant signature. Together, these findings establish TBC1D22B as a regulator of ER-to-Golgi trafficking via RAB1B and implicate it in oncogenic transcriptional remodeling and tumor growth.
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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 Socratic graph.