bims-gerecp Biomed News
on Gene regulatory networks of epithelial cell plasticity
Issue of 2026–06–14
23 papers selected by
Xiao Qin, University of Oxford



  1. Cell Stem Cell. 2026 Jun 09. pii: S1934-5909(26)00227-4. [Epub ahead of print]
      Understanding how cells change state, interact with their neighbors, and organize into tissues requires recording of cellular lineage history in native spatial context. Here, we present SPACE-seq (spatial tracing enabled by CRISPR-based barcodes and slide-seq), a versatile platform that integrates CRISPR-based lineage recording with spatial transcriptomics to jointly resolve lineage, cell state, and tissue architecture at near-cellular resolution in situ. Using SPACE-seq, we uncovered intratumor transcriptional diversification among clonally related cells and identified tumor-stroma crosstalk that reciprocally reshapes behaviors of both malignant and stromal populations, which we further experimentally validated. Beyond disease, SPACE-seq revealed a narrow developmental window in which hepatoblast dispersion contributes to spatially confined lineage compartments that prefigure liver lobar architecture. Together, these results highlight the broad applicability and adaptability of SPACE-seq to uncover previously inaccessible principles of cellular organization, lineage dynamics, and tissue patterning.
    Keywords:  brain development; cellular barcoding; lineage tracing; liver cancer; liver development; spatial transcriptomics
    DOI:  https://doi.org/10.1016/j.stem.2026.05.017
  2. Nat Nanotechnol. 2026 Jun 11.
      Cells operate as networks of proteins, membranes, condensates and compartments, each sensing and displaying distinct intracellular mechanical properties. However, cells also sense, adapt and respond to manifold mechanical properties of the environment, including adhesion, tension, stiffness, shear, viscoelasticity, plasticity, pressure and confinement. By gauging these properties at various timescales and across nano to macro length scales, cellular systems alter their collective responses. The field of mechanobiology aims to elucidate how cellular systems such as tissues, organoids or organs perceive, respond to and influence mechanical cues, and how these impact physiological processes including homeostasis, growth, division, differentiation, movement, development, adaptation and apoptosis. This Perspective highlights challenges within mechanobiology that must be systematically tackled to advance exploration and deepen our understanding of the mechanical attributes of intricate multicellular organisms. Such understanding necessitates the engineering of multicellular models as reference systems, the development of new tools to rigorously quantify and manipulate mechanical properties from the nanoscale to macroscale and theoretical frameworks to decode mechanobiological complexities. Ultimately, addressing these challenges will improve the analysis, monitoring and prediction of mechanobiological processes across molecular, multicellular and organismal scales, thus advancing mechanodiagnostics and mechanomedicine.
    DOI:  https://doi.org/10.1038/s41565-026-02179-0
  3. Cell Genom. 2026 Jun 10. pii: S2666-979X(26)00113-8. [Epub ahead of print]6(6): 101251
      Recent advances in single-cell transcriptomics and CRISPR-based genome editing have enabled large-scale perturbation experiments with genome-wide expression readouts. Single-cell CRISPR screens offer the opportunity to move beyond correlation and estimate causal effects of genetic perturbations on gene expression at scale. These approaches promise to substantially deepen insights into cellular functions and disease mechanisms. However, interpreting statistical associations as causal effects requires additional assumptions beyond those needed for standard statistical analyses. In this minireview, we introduce key concepts and principles for causal effect estimation in trans-regulatory single-cell CRISPR studies. We describe a set of assumptions under which estimates from existing statistical methods admit a causal interpretation and provide a concise overview of these approaches. Finally, through an illustrative example, we demonstrate how violations of these assumptions can bias estimated effects.
    Keywords:  Perturb-seq; causal effect estimation; single-cell CRISPR screens; single-cell transcriptomics
    DOI:  https://doi.org/10.1016/j.xgen.2026.101251
  4. Cancer Cell. 2026 Jun 11. pii: S1535-6108(26)00256-4. [Epub ahead of print]
      In Nature, Buissant des Amorie et al. demonstrate that colorectal cancer acquires oncofetal cell states that resemble embryonic intestines, confer stem-like features, reshape epithelial identity, and prime cells for invasion and metastasis. Oncofetal cells are essential for metastasis and ubiquitous in non-metastatic tumors, with cancer-associated fibroblasts as key microenvironmental drivers.
    DOI:  https://doi.org/10.1016/j.ccell.2026.05.011
  5. Nat Genet. 2026 Jun;58(6): 1331-1340
      Colorectal cancer (CRC) frequently harbors activating mutations in the WNT and MAPK pathways. While KRAS mutations alone can drive tumor initiation in many tissues, they are insufficient in the intestine. Leveraging allele-specific properties of RAS, we developed a mouse model to investigate MAPK hyperactivation. Here we show that KRAS mutations drive a regenerative state while antagonizing the Lgr5+ intestinal stem cell state; however, this regenerative state cannot initiate tumorigenesis. Instead, tumor initiation requires a stem-like state dependent on mutational activation of the WNT pathway. We identify two aberrant states-a WNT-driven stem-like state for tumor initiation and MAPK-driven transit-amplifying-like state for tumor growth. These plastic states, essential for tumorigenesis, also impact drug response, potentially explaining lower response rates and shorter duration of response to KRAS-G12C inhibitors in CRC compared to non-small cell lung cancer. These findings highlight the need to target both pathways and their associated cell states for effective CRC treatment.
    DOI:  https://doi.org/10.1038/s41588-026-02611-0
  6. Nature. 2026 Jun 08.
      Genetic mutations that drive cancer often occur in tumor suppressor proteins, including the p53 transcription factor which is altered in ~40-50% of cases1,2. However, current therapies fail to target most such mutations because the mutant proteins typically lack defined drug-binding pockets, and restoring the endogenous function has proven challenging. Here, we programmed CRISPR-Cas12a2, an RNA-guided nuclease with trans-nucleolytic cleavage activities3,4, to selectively kill cancer cells by targeting cancer-specific transcripts. This approach limits cell growth by inducing trans shredding of chromatin, triggering DNA damage responses and cell death. Unlike existing methods, RNA-guided Cas12a2 senses cellular RNA signatures, enabling precise targeting of undruggable mutations. Transcript-activated chromatin shredding provides a new approach to precision disease treatments for undruggable targets.
    DOI:  https://doi.org/10.1038/s41586-026-10738-7
  7. bioRxiv. 2026 Jun 03. pii: 2026.05.31.729161. [Epub ahead of print]
      Cancer arises from extensive genetic and epigenetic alterations that reshape chromatin, transcriptional regulation, and malignant cell states. To systematically chart cancer-intrinsic regulatory programs, we constructed a pan-cancer single-cell transcriptomic and epigenomic atlas encompassing 60 human cell lines representing 16 tissue origins and 20 cancer types, comprising 240,957 single-nucleus RNA-seq and 223,347 single-nucleus ATAC-seq profiles. Integrative analyses revealed extensive pan-cancer cell-state heterogeneity, core gene-regulatory networks, and a conserved epithelial-mesenchymal transition (EMT) axis that transcends tissue of origin. Copy-number variation analysis identified transcription factor amplification and downstream hyperactivation as key drivers of cancer cell-state reprogramming. To further examine how regulatory programs diverge within a cancer lineage and contribute to clinically divergent outcomes, we performed a focused comparison of cutaneous melanoma with acral melanoma, a rare, UV-independent subtype underrepresented in existing pan-cancer atlases. The comparison uncovered a universal inflammation-suppressive program in acral melanoma and an inflamed regulatory landscape in cutaneous melanoma, with the JAK-STAT pathway and downstream transcriptional responses as central discriminators. Integration of single-cell and bulk datasets across models and patient cohorts further linked in vitro tumor-intrinsic gene regulations with in vivo microenvironmental composition and immunotherapy responses. Together, by extending single-cell multi-omic profiling to rare alongside common cancer subtypes, this atlas offers a resource for mapping pan-cancer and subtype-specific gene-regulatory programs that shape cancer cell-state plasticity.
    DOI:  https://doi.org/10.64898/2026.05.31.729161
  8. bioRxiv. 2026 Jun 05. pii: 2026.06.02.729594. [Epub ahead of print]
      Integrating single-cell transcriptomic and epigenomic data provides a robust framework for investigating gene regulation mechanisms. Existing analyses typically treat these modalities as synchronized features that can be translated in a static manner; however, the temporal delays that underpin cellular kinetics are intrinsic to dynamic biological systems. To address this limitation, we propose utilizing the "molecular asynchrony" within regulatory hierarchies to determine the thermodynamic properties of individual cells. Here, we present SeqTag, a single-cell multiomics sequencing method that simultaneously profiles the transcriptome, chromatin accessibility, and histone modifications, supported by an analytical framework to identify asynchronous states across regulatory layers for characterization of single-cell kinetics. By measuring the epigenetic priming potential and remodeling rates during adult mouse oligodendrogenesis, we delineated a sequential program for bivalency resolution as maturing cells traverse Waddington's landscape. This process becomes increasingly decoupled with age, a change linked to a drift in progenitor cell-fate probabilities. By identifying entropy-driving regulatory elements, we characterized the aging-related decline in cell identity across various cell types and proposed a dynamic model linking static genetic variants to the risk of late-onset diseases. In summary, our integrated approach established a unified framework for employing multimodal single-cell genomics to model the kinetics of complex cellular processes.
    DOI:  https://doi.org/10.64898/2026.06.02.729594
  9. Cancer Cell. 2026 Jun 11. pii: S1535-6108(26)00255-2. [Epub ahead of print]
      In this issue of Cancer Cell, Alonso et al. demonstrate that in patients with advanced colorectal cancer, there are regionally distinct genomic and transcriptomic adaptive responses to KRAS G12C inhibition, including epithelial cell state changes and pro-inflammatory pathway enrichment, and provide insights into key resistance mechanisms to KRAS G12C inhibition.
    DOI:  https://doi.org/10.1016/j.ccell.2026.05.010
  10. Cancer Cell. 2026 Jun 11. pii: S1535-6108(26)00258-8. [Epub ahead of print]
      In this issue of Cancer Cell, Liu et al. use mitochondrial DNA mutations to reconstruct clonal lineages of the innate immune compartment in human tumors. They show that intratumoral type 3 dendritic cells (DC3s) arise from circulating monocytes and that a monocyte's fate in the tumor microenvironment is programmed peripherally, prior to tissue entry.
    DOI:  https://doi.org/10.1016/j.ccell.2026.05.013
  11. Science. 2026 Jun 11. eadv8291
      The identification of the cancer cell of origin is a fundamental question in cancer biology. We used fluorescent lineage tracing of independent mouse skin stem cell populations, single cell transcriptomics, and Duplex sequencing, to identify the origin of chemically induced skin tumors. Tumors arose predominantly from Lgr6+ and / or Lrig1+ stem cells of the upper hair follicle, but only very rarely from the Lgr5+ and Krt19+ hair follicle bulge. Lgr6+ stem cells initiated by dimethylbenzanthracene responded to tumor promoter treatment resulting in clonal expansion of initiated cells carrying the canonical Hras Q61L mutation. Spontaneous mutations in Kras also clonally expanded, but did not generate tumors unless the Hras gene was deleted, thus revealing a competitive interaction between Hras and Kras pathways that influences clonal selection.
    DOI:  https://doi.org/10.1126/science.adv8291
  12. bioRxiv. 2026 Jun 02. pii: 2026.06.01.729390. [Epub ahead of print]
      CRISPR interference screens use catalytically inactive dCas9 fused to a repressor domain to enable genetic perturbations at the transcriptomic level. Interpretation of results involves identification of guide RNAs associated with the screen phenotype, followed by secondary analysis. During validation of a genetic screen, we observed different phenotypes from non-overlapping guide RNAs targeting one gene. Here, we developed POCKET-seq to map the binding of dCas9 genome-wide. We show that off-target binding occurs frequently and can generate false-positive interactions when it occurs near the promoter of genes associated with the screen phenotype. POCKET-seq classifies these false-positive and true-positive interactions using gene ontology.
    DOI:  https://doi.org/10.64898/2026.06.01.729390
  13. Cell. 2026 Jun 11. pii: S0092-8674(26)00587-8. [Epub ahead of print]189(12): 3501-3505
    NIH SenNet consortium
      Cellular senescence comprises diverse cell states emerging across human tissues during aging and disease. Integrating single-cell and spatial multi-omics with AI-driven analyses enables systematic mapping of senescent cell heterogeneity ("senotypes"), revealing tissue-specific programs and microenvironmental interactions. These advances provide frameworks for biomarker discovery and development of targeted senotherapeutic strategies.
    DOI:  https://doi.org/10.1016/j.cell.2026.05.028
  14. Trends Cancer. 2026 Jun 11. pii: S2405-8033(26)00108-1. [Epub ahead of print]
      Early-life exposure to both modifiable and nonmodifiable risk factors may induce chronic low-grade inflammation (CLGI), a silent threat potentially driving the rising incidence of early-onset colorectal cancer (EOCRC). Notably, CLGI could promote EOCRC by altering the proinflammatory and immune microenvironment that supports tumor growth and cancer development. In this review, we examine how risk factors disrupt immune homeostasis and contribute to CLGI in young individuals, thereby promoting the development of EOCRC. Additionally, identifying CLGI-specific biomarkers could aid in early detection and diagnosis, while targeting specific molecular pathways may enable personalized therapeutic interventions for EOCRC by reducing the chronic inflammatory threat. We also highlight the importance of lifestyle changes and interventions to reduce CLGI and address the growing health concern of EOCRC.
    Keywords:  chronic low-grade inflammation; early-onset colorectal cancer; exposomes; inflammatory biomarkers; microbiome dysbiosis
    DOI:  https://doi.org/10.1016/j.trecan.2026.05.005
  15. Cell. 2026 Jun 11. pii: S0092-8674(26)00588-X. [Epub ahead of print]189(12): 3511-3512
      RNA velocity can predict the direction of cell-state change, but the regulatory programs shaping these changes remain difficult to identify. In this issue of Cell, Wang et al. introduce RegVelo, a framework that integrates gene regulatory networks into RNA velocity analysis to nominate candidate regulators that may bias cell fate.
    DOI:  https://doi.org/10.1016/j.cell.2026.05.029
  16. Trends Cancer. 2026 Jun 12. pii: S2405-8033(26)00125-1. [Epub ahead of print]
      Aging is a major risk factor for cancer, yet its role in cancer biology remains largely unexplored and often overlooked. Interestingly, studies assessing the impact of aging on oncogenic KrasG12D-driven lung tumor initiation, early progression, and metastasis have reported both pro- or antitumoral effects, which are presented and discussed herein.
    Keywords:  aging; cancer; lung; tumorigenesis
    DOI:  https://doi.org/10.1016/j.trecan.2026.05.007
  17. J Natl Cancer Cent. 2026 Jun;6(3): 211-218
      Metastatic relapse is frequently driven by dormant disseminated tumor cells (DTCs) that previously evaded initial therapy, disseminated to distant tissues, entered into a non-proliferative state termed dormancy, and later reawakened to reinitiate active proliferation and the outgrowth of macroscopic metastases. Cancer dormancy manifests itself in two principal forms: cellular dormancy, characterized by the reversible, proliferative quiescence of individual cells, and tumor mass dormancy, defined by a balance between proliferation and compensating cell death. Dormant cells are notably resistant to conventional therapies and immune-mediated clearance, yet retain viability and the potential to re-enter the active cell cycle. The present review focuses on dormancy of DTCs residing in distant tissues and highlights recent advances in our understanding of both cell-intrinsic and -extrinsic regulators of cancer dormancy. Key cell-autonomous mechanisms include ERK/p38 signaling ratios, epithelial-mesenchymal plasticity, and Wnt signaling. At the same time, signals received by dormant DTCs from the adjacent tissue microenvironment-such as TGF-β family cytokines, immune surveillance, and other stromal interactions-induce and sustain dormancy. Importantly, emerging evidence suggests that microenvironmental conditions, including inflammation and aging, can trigger the awakening of dormant DTCs, leading to metastatic outgrowth. We review these evolving insights into the molecular and environmental control of cancer dormancy and awakening, underscoring their clinical relevance and therapeutic potential in preventing metastatic recurrence.
    Keywords:  Cancer dormancy and awakening; Disseminated tumor cells; Epithelial-mesenchymal plasticity; Metastasis; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.jncc.2026.03.007
  18. Cell Stem Cell. 2026 Jun 08. pii: S1934-5909(26)00196-7. [Epub ahead of print]
      Principles of developmental biology have inspired efforts for directed differentiation of human pluripotent stem cells (hPSCs), leading to the first generation of organoids that are now well established as models of human development and disease. However, first-generation organoid models were missing many cell types that would be needed to study normal and pathological processes. Here, we discuss how designing next-generation organoids with increased cellular complexity has been possible by better reproducing developmental processes in play during organogenesis in vivo. We focus on recent conceptual and technical advances in reconstructing appropriate cellular diversity in organoids, dissecting the importance of tissue-tissue interactions and specialized cell addition, and how engineering technologies can further enhance our ability to control how cells are brought together to mimic human development in vitro.
    Keywords:  assembloid; developmental biology; engineering organoid; organogenesis; organoid; self-organization
    DOI:  https://doi.org/10.1016/j.stem.2026.05.004
  19. Nat Genet. 2026 Jun;58(6): 1396-1408
      Cells communicate through ligand-receptor (LR) signaling interactions, but identifying when and where these interactions are active remains challenging. We developed CytoSignal to infer the locations and dynamics of cell-cell communication at cellular resolution from spatial transcriptomic data. Here we show that our cellular resolution, spatially resolved signaling scores enable several important analyses-identifying spatial gradients in signaling strength, quantifying the locations of contact-dependent and diffusible interactions, detecting signaling-associated genes and identifying differential signaling across multisample data. Additionally, we can predict the temporal dynamics of a signaling interaction at each spatial location. We experimentally validate our results in situ by proximity ligation assay, confirming that CytoSignal predicts the locations of LR interactions more accurately than previous approaches. This study addresses the field's current need for a robust and scalable tool to detect cell-cell signaling interactions and their dynamics at cellular resolution from spatial transcriptomic data.
    DOI:  https://doi.org/10.1038/s41588-026-02624-9
  20. Proc Natl Acad Sci U S A. 2026 Jun 16. 123(24): e2528450123
      The mechanisms by which Wnt/β-catenin signaling regulates gene expression in a tissue- and context-specific manner remain poorly understood, limiting our ability to target the aberrant cell growth typical of many Wnt-driven cancers. Here, we focus on malignant liver tumors driven by activating CTNNB1 (β-catenin) mutations that nevertheless display distinct phenotypic states and Wnt outputs. By profiling patient-derived organoids via single-cell transcriptomics and chromatin dynamics, we identify subtype-specific transcriptional and epigenetic profiles. Using CUT&RUN, we show that β-catenin engages distinct genomic regions, dictated by differential association with TCF/LEF family transcription factors. Specifically, we define a sequence-specific regulatory element engaged by β-catenin only upon interaction with TCF7L2, revealing that partner choice, independent of CTNNB1 mutational status, ultimately determines cell fate. Our findings, validated across multiple tumor models and patient tissues, offer a framework for understanding how differential β-catenin-TCF/LEF interaction orchestrates context-specific Wnt signaling outcomes.
    Keywords:  TCF/LEF; Wnt signaling; cancer; novel motif; β-catenin
    DOI:  https://doi.org/10.1073/pnas.2528450123
  21. Trends Immunol. 2026 Jun 09. pii: S1471-4906(26)00129-8. [Epub ahead of print]
      Immune-mediated inflammatory disorders, such as inflammatory bowel diseases, are characterized by chronic inflammation and damage to the intestinal barrier. Several of the current therapeutic strategies for inflammatory diseases attempt to decrease inflammation but cause side effects in a significant fraction of patients without promoting remission. Leveraging the power of intestinal regeneration for therapeutic purposes holds great promise, but it comes with the significant risk of promoting tumorigenesis, as most of the pathways that boost the regenerative program are also exploited by tumor cells for their growth and survival. In this article, we review the common mechanisms promoting intestinal regeneration and tumor development and discuss the latest studies identifying cellular and molecular pathways that promote regeneration but not tumorigenesis.
    Keywords:  colorectal cancer; inflammatory bowel disease; mucosal healing; regeneration; tumorigenesis
    DOI:  https://doi.org/10.1016/j.it.2026.05.004
  22. Front Immunol. 2026 ;17 1792954
      Colorectal cancer (CRC) is one of the most commonly occurring malignancies worldwide, with incidence and mortality rising sharply in older adults. While aging is increasingly recognized as a key risk factor for CRC, the fundamental immunological mechanisms which underlie this risk remain incompletely understood. Two interconnected processes, namely inflammaging and immunosenescence, appear central to this association. On the one hand, inflammaging, which is characterized by chronic low-grade inflammation in older individuals, fosters a tumor-promoting microenvironment through oxidative stress, genomic instability, and persistent cytokine activation. On the other hand, immunosenescence diminishes immune surveillance, reducing the clearance of premalignant cells and weakening responses to tumor progression and therapy. Together, these processes create an immunological framework that predisposes the aging colon to malignant transformation. This review synthesizes current knowledge of the cellular and mechanistic impacts of inflammaging and immunosenescence in CRC pathogenesis, highlighting their roles in shaping disease susceptibility in the elderly. These insights may guide future endeavor in biomarker discovery, prevention, and therapeutic intervention to mitigate the burden of CRC in aging populations.
    Keywords:  aging; colorectal cancer; immunosenescence; inflammaging; mechanism
    DOI:  https://doi.org/10.3389/fimmu.2026.1792954