bims-pideca Biomed News
on Class IA PI3K signalling in development and cancer
Issue of 2026–01–18
thirteen papers selected by
Ralitsa Radostinova Madsen, MRC-PPU



  1. Proc Natl Acad Sci U S A. 2026 Jan 20. 123(3): e2501779123
      In metazoans, epithelia perform functions of absorption, diffusion, and secretion. The actin-based apical projections on the epithelial cells contribute to these functions and are formed via cell-autonomous mechanisms that control cell polarity, intracellular transport, and the cytoskeleton. However, the cues that function upstream of these cell-autonomous regulators remain poorly known. Using microridges on zebrafish epithelial cells as a paradigm, we show that mTOR, a metabolic sensor, regulates the formation of apical projections. Mechanistically, mTORC1 controls the RhoA-ROCK activity via S6K1 to prevent the overactivation of nonmuscle myosin II (NMII) to restrict microridge elongation. Furthermore, genetic, biochemical, and molecular dynamics simulation analyses reveal that mTORC2 regulates the microridge pattern by modulating the activity of aPKC via its differential phosphorylation at two conserved sites. We propose that mTOR integrates the developmental and/or metabolic status of epithelial cells with cell autonomously acting RhoA and aPKC to regulate tissue-wide formation of apical projections.
    Keywords:  RhoA signaling; aPKC signaling; actin cytoskeleton; mTOR signaling; microridges
    DOI:  https://doi.org/10.1073/pnas.2501779123
  2. bioRxiv. 2026 Jan 09. pii: 2026.01.09.698608. [Epub ahead of print]
      Single-cell transcriptomics offers the promise of measuring the diversity of cellular phenotypes across species, diseases, and other biological conditions. Recently, foundation models have emerged to identify this variation, yet most methods represent each cell independently, despite technical limitations that reduce measurement precision at the single-cell level. Here, we present S tack , a foundation model trained on 149 million uniformly preprocessed human single cells that leverages tabular attention to generate representations for each cell informed by the cells in its context. S tack offers substantial improvements for downstream tasks in the zero-shot setting compared to baselines, whether they are zero-shot, fine-tuned, or trained from scratch on the target dataset. S tack can perform in-context learning from unlabeled cells representing arbitrary conditions, such as a chemical perturbation or a different donor, and predict the effect of those conditions on a target cell population without requiring data-specific fine-tuning. We apply S tack to generate Perturb Sapiens , the first human whole-organism atlas of perturbed cells, spanning 28 tissues, 40 cell classes, and 201 perturbations. We validated subsets of Perturb Sapiens using in vitro stimulation profiles. Overall, S tack presents a new modeling framework where cells themselves act as guiding examples at inference time, unlocking general-purpose in-context learning capabilities for single-cell biology.
    DOI:  https://doi.org/10.64898/2026.01.09.698608
  3. Science. 2026 Jan 15. eadz9353
      Understanding how cells make decisions over time requires the ability to link past molecular states to future phenotypic outcomes. We present TimeVault, a genetically encoded system that records and stores transcriptomes within living mammalian cells for future readout. TimeVault leverages engineered vault particles that capture mRNA through poly(A) binding protein. We demonstrate that the transcriptome stored by TimeVaults is stable in living cells for over 7 days. TimeVault enables high-fidelity transcriptome-wide recording with minimal cellular perturbation, capturing transient stress responses and revealing gene expression changes underlying drug-naive persister states in lung cancer cells that evade EGFR inhibition. By linking past and present cellular states, TimeVault provides a powerful tool for decoding how cells respond to stress, make fate decisions, and resist therapy.
    DOI:  https://doi.org/10.1126/science.adz9353
  4. bioRxiv. 2026 Jan 07. pii: 2026.01.07.698128. [Epub ahead of print]
      Oncogenic KRAS and NRAS mutations are common in hematologic malignancies, but how they signal is less well characterized than in carcinomas. To uncover novel RAS biology and potential therapeutic vulnerabilities, we employed a multi-omics screening approach in multiple myeloma to identify regulators of RAS activity. We report that the phosphatase PP1C dephosphorylates the conserved T148 residue on RAS, which in turn permits LZTR1-dependent proteasomal degradation. Notably, LZTR1 is ineffective against KRAS A146 gain-of-function mutations, which are adjacent to T148 and prevalent in hematologic cancers. Remarkably, we find that KRAS protein is four-fold less stable in hematologic versus carcinoma cells, offering a unique therapeutic opportunity targeting RAS protein stability mechanisms. The kinases PAK1 and PAK2 shield RAS from LZTR1-dependent degradation by phosphorylating T148, and targeting PAK1/2 activity improves RAS-directed therapy. Collectively, our findings reveal a novel regulatory circuit governing RAS stability that is preferentially active in blood cancers and potentially druggable.
    DOI:  https://doi.org/10.64898/2026.01.07.698128
  5. J Dermatol. 2026 Jan 14.
      Vascular anomalies are classified according to the ISSVA classification into vascular tumors with endothelial proliferation and vascular malformations without proliferation. Infantile hemangioma is a vascular tumor that is diagnosed by GLUT-1 immunoreactivity. GLUT-1 positivity is reportedly sometimes observed in angiosarcoma, but the clinical significance remains unclear. Here, immunohistochemistry was performed on tissue samples from patients with angiosarcoma (n = 10), pyogenic granuloma (n = 9), and senile hemangioma (n = 10), with infantile hemangioma serving as a positive control. GLUT-1 expression was detected in the cytoplasm and/or cell membrane of tumor cells in all cases of angiosarcoma (100%), as well as in the cytoplasm of some cases of pyogenic granuloma (44.4%) and senile hemangioma (40%). Double immunofluorescent staining for GLUT-1 and CD34 revealed co-expression in tumor endothelial cells of angiosarcoma. Clinically, cases of angiosarcoma with strong membranous GLUT-1 expression tended to be associated with tumor progression, while those with weak or mild cytoplasmic expression showed a better response to treatment. These findings suggest that GLUT-1 may serve as a useful marker of tumor progression for angiosarcoma, and as a potential therapeutic target in vascular tumors.
    Keywords:  GLUT‐1; angiosarcoma; immunohistochemistry
    DOI:  https://doi.org/10.1111/1346-8138.70147
  6. Genome Biol. 2026 Jan 10.
      Differential expression is a key application of imaging spatial transcriptomics, moving analysis beyond cell type localization to examining cell state responses to microenvironments. However, spatial data poses new challenges to differential expression: segmentation errors cause bias in fold-change estimates, and correlation among neighboring cells leads standard models to inflate statistical significance. We find that ignoring these issues can result in considerable false discoveries that greatly outnumber true findings. We present a suite of solutions to these fundamental challenges, and implement them in the R package smiDE.
    Keywords:  Differential expression; Segmentation error mitigation; Spatial correlation; Spatial random effects model; Spatial transcriptomics
    DOI:  https://doi.org/10.1186/s13059-025-03867-1
  7. Nat Chem Biol. 2026 Jan 13.
      The Warburg effect leads to increased lactate production and promotes cancer progression but the underlying mechanisms remain unclear. Here, we found that lactate activates the MAPK pathway through ERK lactylation, which promotes cancer progression. We identified GCN5 as the lactyltransferase responsible for ERK lactylation. Activated ERK phosphorylates GCN5, increasing its lactyltransferase activity toward ERK and establishing a positive feedback loop that amplifies lactate-mediated cancer progression. We provide evidence that lactylation of ERK at residue K231 weakens its interaction with MEK, thereby promoting ERK dimerization and activation. We developed a cell-penetrating peptide that specifically inhibits ERK lactylation. This peptide impairs tumor growth in KRAS-mutant cancer models. Taken together, our findings reveal a molecular mechanism by which lactate accelerates cancer progression through the ERK-GCN5 lactylation-phosphorylation cascade and suggest a strategy to disrupt ERK lactylation in RAS-ERK-driven cancers.
    DOI:  https://doi.org/10.1038/s41589-025-02107-8
  8. bioRxiv. 2026 Jan 07. pii: 2026.01.06.698060. [Epub ahead of print]
      Recent years have seen rapid growth in single-cell foundation models (scFMs), raising expectations for transformative advances in genomic data analysis. However, their adoption has been hindered by inconsistent performance across datasets, fragmented software ecosystems, high technical barriers, and the lack of best practices established through systematic, reproducible benchmarks. Here we present a unified, extensible, and fully automated computational framework that standardizes the execution, evaluation, and extension of diverse scFMs. The framework harmonizes software environments, eliminates manual configuration, and enables large-scale, reproducible evaluation across heterogeneous datasets and training regimes. Leveraging this infrastructure, we systematically benchmark thirteen foundation models alongside classical baselines across more than fifty datasets under zero-shot, few-shot, and fine-tuning settings. We show that pretrained embeddings capture biologically meaningful structure and provide clear advantages in low-label and transfer-learning scenarios, while classical PCA approach remains competitive or even preferable in others. Together, this work lowers technical barriers, delivers best practices, and establishes a transparent and reproducible standard for community-wide evaluation, accelerating rigorous development and adoption of scFMs.
    DOI:  https://doi.org/10.64898/2026.01.06.698060
  9. J Am Chem Soc. 2026 Jan 13.
      Proteolysis-targeting chimeras (PROTACs) have transformed the concept of chemical intervention in biological systems by co-opting the ubiquitin-proteasome system to selectively degrade proteins. A key promise of this modality is that proximity alone─not inhibition─is required, allowing binding anywhere on the protein surface to trigger degradation. Yet despite this conceptual freedom, most PROTACs to date have been built from orthosteric inhibitors. The use of allosteric or functionally silent ligands remains a largely untapped opportunity. In this Perspective, we spotlight pioneering efforts in allosteric PROTAC design and explore how such strategies could unlock improved outcomes for target selectivity, efficacy, and resistance management while also modulating physicochemical properties to enhance in vivo performance. We further discuss the practical and conceptual challenges and the advances needed to make allosteric targeting a mainstream strategy in the design of protein degraders and other proximity-inducing molecules.
    DOI:  https://doi.org/10.1021/jacs.5c14840
  10. Sci Rep. 2026 Jan 12.
      We found that healthy mice harbor T cells with heritable low Pten expression and that monoallelic Pten loss in CD4 T cells causes a bias in their differentiation toward T follicular helper cells during acute viral infection. These results suggest that somatically induced mono- or biallelic loss of expression of signaling-related genes in T cells can impact the quality of population-level T cell responses-without conspicuous pathological sequelae such as autoimmune and inflammatory manifestations or lymphomagenesis.
    DOI:  https://doi.org/10.1038/s41598-025-34754-1
  11. ArXiv. 2026 Jan 07. pii: arXiv:2601.01850v2. [Epub ahead of print]
      Allostery is a fundamental mechanism of protein regulation and is commonly interpreted as modulating enzymatic activity or product abundance. Here we show that this view is incomplete. Using a stochastic model of allosteric regulation combined with an information-theoretic analysis, we quantify the mutual information between an enzyme's regulatory state and the states of downstream signaling components. Beyond controlling steady-state production levels, allostery also regulates the timing and duration over which information is transmitted. By tuning the temporal operating regime of signaling pathways, allosteric regulation enables distinct dynamical outcomes from identical molecular components, providing a physical mechanism for temporal information flow, signaling specificity, and coordination without changes in metabolic pathways.