bims-instec Biomed News
on Intestinal stem cells and chemoresistance in colon cancer and intestinal regeneration
Issue of 2025–04–13
thirteen papers selected by
Maria-Virginia Giolito, Université Catholique de Louvain



  1. Cell Stem Cell. 2025 Apr 01. pii: S1934-5909(25)00095-5. [Epub ahead of print]
      Enterocytes and four classic secretory cell types derive from intestinal epithelial stem cells. Based on morphology, location, and canonical markers, goblet and Paneth cells are considered distinct secretory types. Here, we report high overlap in their transcripts and sites of accessible chromatin, in marked contrast to those of their enteroendocrine or tuft cell siblings. Mouse and human goblet and Paneth cells express extraordinary fractions of few antimicrobial genes, which reflect specific responses to local niches. Wnt signaling retains some ATOH1+ secretory cells in crypt bottoms, where the absence of BMP signaling potently induces Paneth features. Cells that migrate away from crypt bottoms encounter BMPs and thereby acquire goblet properties. These phenotypes and underlying accessible cis-elements interconvert in post-mitotic cells. Thus, goblet and Paneth properties represent alternative phenotypic manifestations of a common signal-responsive terminal cell type. These findings reveal exquisite niche-dependent cell plasticity and cis-regulatory dynamics in likely response to antimicrobial needs.
    Keywords:  Paneth cells; epigenetic control of cell properties; goblet cells; intestinal epithelial differentiation; intestinal stem cells; lineage plasticity
    DOI:  https://doi.org/10.1016/j.stem.2025.03.005
  2. Nat Commun. 2025 Apr 05. 16(1): 3264
      Understanding the molecular mechanisms that regulate intestinal epithelial cell (IEC) renewal provides potential targets for inflammatory bowel disease (IBD). Growing evidence has highlighted the importance of epithelial signals in regulating intestinal stem cell (ISC) differentiation. However, it remains unclear which IEC-derived cytokines can precisely regulate ISC commitment toward specific mature cells. Here we systematically analyze all fibroblast growth factors (FGFs) expression and find that colonic FGF1 levels are inversely correlated with the severity of IBD in mouse models and patients. IEC-specific Fgf1 deletion leads to impaired goblet cell differentiation and exacerbated colitis, while pharmacological administration of recombinant FGF1 (rFGF1) alleviates colitis by enhancing goblet cell differentiation and improving colonic epithelial integrity. Mechanistic studies reveal that rFGF1 directs ISC differentiation toward goblet cells via FGFR2-TCF4-ATOH1 signaling axis. In conclusion, our study identifies an epithelial niche-derived FGF1 that regulates ISC commitment toward goblet cells, shedding light on strategies for treating IBD.
    DOI:  https://doi.org/10.1038/s41467-025-58644-2
  3. Oncogene. 2025 Apr 06.
      Colorectal cancer (CRC) can be divided into 4 subtypes of which consensus molecular subtype 4 (CMS4) is associated with metastasis and poor survival. Previously, we reported that the KPN mouse model resembles human CMS4. Strikingly, although tumor formation in this model is slow and limited, effective metastasis is observed. To understand this aggressive behavior, we compared two distinct in vitro KPN models, organoids and tumoroids. The organoid model only carries the original mutations, while the tumoroids are derived from in vivo grown tumors that underwent selection during development. Here, we reveal that tumoroids harbor endogenous WNT pathway activity, which can be driven by tankyrase activity and Cdx2 downregulation. Importantly, WNT pathway activation was heterogeneous in nature, subject to regulation and allowed for a mixture of WNT-driven and YAP-driven cells within tumoroids. This unique type of WNT pathway activation is not crucial for colonic tumor growth, but results in metastatic spreading. Intriguingly, these findings reflect a specific subset of aggressive human CMS4 cancers that display low CDX2 expression and lack of classical WNT pathway mutations, while having a higher tendency to metastasize. Together, these data propose a novel mechanism for WNT pathway activation that drives metastasis formation in aggressive CRC.
    DOI:  https://doi.org/10.1038/s41388-025-03365-5
  4. J Pathol. 2025 Apr 11.
      Colorectal cancer (CRC) is the third most common form of cancer globally, and arises from the hyperproliferation of epithelial cells in the intestine. The architecture and maintenance of these cells is governed by two major signalling pathways working in a counter-gradient: the stem cell WNT signalling pathway, and the prodifferentiation bone morphogenetic protein (BMP) pathway. It has long been known that this WNT-BMP balance is disrupted in CRC, with hyperactive WNT signalling leading to increased proliferation of epithelial cells and tumour progression. BMP signalling, and its prodifferentiation effects, have increasingly become a focus for CRC research. Loss of BMP signalling, and that of its receptors, has been shown to increase WNT signalling and cancer stem cells in CRC. BMP signalling is further modulated through secreted BMP antagonists localised to the intestinal crypts, which create a niche ensuring that sustained WNT signalling can maintain stem-cell self-renewal capacity. A number of studies combine to demonstrate the effects of overexpression of these BMP antagonists, showing that hyperactivity of the stem-cell-supporting WNT signalling pathway ensues, leading to deregulation of the intestinal epithelium. Cellular hyperproliferation, the emergence of ectopic crypts, and an increase in stem cell numbers and characteristics are common themes, contributing to disrupted epithelial homeostasis, an increase in CRC risk and progression, and resistance to therapy. This review aims to compile the current knowledge on BMP antagonists, their role in CRC development, and how we can utilise this information for biomarker research and novel therapeutics. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
    Keywords:  BMP; BMP antagonists; WNT; cancer stem cells; cellular plasticity; colorectal cancer
    DOI:  https://doi.org/10.1002/path.6428
  5. Cell Death Differ. 2025 Apr 09.
      The stress-associated chaperone system is an actionable target in cancer therapies. It is ubiquitously upregulated in cancer tissues and enables tumorigenicity by stabilizing oncoproteins. Most inhibitors target the key component, heat-shock protein 90 (HSP90). Although HSP90 inhibitors are highly tumor-selective, they fail in clinical trials. These failures are partly due to interference with a negative regulatory feedback loop in the heat-shock response (HSR): in response to HSP90 inhibition, there is compensatory synthesis of stress-inducible chaperones, mediated by the transcription factor heat-shock-factor 1 (HSF1). We recently identified that wild-type p53 reduces the HSR by repressing HSF1 via a p21-CDK4/6-MAPK-HSF1 axis. Here, we test whether in HSP90-based therapies, simultaneous p53 activation or direct cell cycle inhibition interrupts the deleterious HSF1-HSR axis and improves the efficiency of HSP90 inhibitors. We found that the clinically relevant p53 activator Idasanutlin suppresses the HSF1-HSR activity in HSP90 inhibitor-based therapies. This combination synergistically reduces cell viability and accelerates cell death in p53-proficient colorectal cancer (CRC) cells, murine tumor-derived organoids, and patient-derived organoids (PDOs). Mechanistically, upon combination therapy, CRC cells upregulate p53-associated pathways, apoptosis, and inflammatory pathways. Likewise, in a CRC mouse model, dual HSF1-HSP90 inhibition represses tumor growth and remodels immune cell composition. Importantly, inhibition of the cyclin-dependent kinases 4/6 (CDK4/6) under HSP90 inhibition phenocopies synergistic repression of the HSR in p53-proficient CRC cells. Moreover, in p53-deficient CRC cells, HSP90 inhibition in combination with CDK4/6 inhibitors similarly suppresses the HSF1-HSR and reduces cancer growth. Likewise, p53-mutated PDOs respond to dual HSF1-HSP90 inhibition, providing a strategy to target CRC independent of the p53 status. In sum, we provide new options to improve HSP90-based therapies to enhance CRC therapies.
    DOI:  https://doi.org/10.1038/s41418-025-01502-x
  6. Cell Death Dis. 2025 Apr 05. 16(1): 253
      The extent of mitochondrial heterogeneity and the presence of mitochondrial archetypes in cancer remain unknown. Mitochondria play a central role in the metabolic reprogramming that occurs in cancer cells. This process adjusts the activity of metabolic pathways to support growth, proliferation, and survival of cancer cells. Using a panel of colorectal cancer (CRC) cell lines, we revealed extensive differences in their mitochondrial composition, suggesting functional specialisation of these organelles. We differentiated bioenergetic and mitochondrial phenotypes, which point to different strategies used by CRC cells to maintain their sustainability. Moreover, the efficacy of various treatments targeting metabolic pathways was dependent on the respiration and glycolysis levels of cancer cells. Furthermore, we identified metabolites associated with both bioenergetic profiles and cell responses to treatments. The levels of these molecules can be used to predict the therapeutic efficacy of anti-cancer drugs and identify metabolic vulnerabilities of CRC. Our study indicates that the efficacy of CRC therapies is closely linked to mitochondrial status and cellular bioenergetics.
    DOI:  https://doi.org/10.1038/s41419-025-07596-y
  7. Tissue Eng Part B Rev. 2025 Apr 08.
      Colorectal cancer (CRC) recurs at a striking rate, specifically in patients with liver metastasis. Dormant CRC cells disseminated following initial primary tumor resection or treatment often resurface years later to form aggressive, therapy-resistant tumors that result in high patient mortality. Routine imaging-based screenings often fail to detect dormant cancer cell clusters, and there are no overt symptomatic presentations, making dormant CRC a major clinical challenge to diagnose and treat. Tissue engineering approaches are ideally suited to model dormant cancer cells and enable the discovery of therapeutic vulnerabilities or unique mechanistic dependencies of dormant CRC. Emerging evidence suggests that tissue-engineered approaches have been successfully used to model dormant breast and lung cancer. With CRC responsible for the second most cancer-related deaths worldwide and CRC patients commonly experiencing recurrence, it is essential to expand dormancy models to understand this phenomenon in the context of CRC. Most published in vitro models of CRC dormancy simplify the complex tumor microenvironment with two-dimensional culture systems to elucidate dormancy-driving mechanisms. Building on this foundation, future research should apply tissue engineering methods to this growing field to generate competent three-dimensional models and increase mechanistic knowledge. This review summarizes the current state of in vitro CRC dormancy models, highlighting the techniques utilized to give rise to dormant CRC cells: nutrient depletion, anticancer drugs, physical extracellular matrix interactions, and genetic manipulation. The metrics used to validate dormancy within each model are also consolidated to demonstrate the lack of established standards and the ambiguity around comparing studies that have been validated differently. The methods of these studies are organized in this review to increase comprehensibility and identify needs and opportunities for future bioengineered in vitro models to address dormancy-driven mortality in patients with CRC liver metastasis. Impact Statement Dormant cancer drives high patient mortality, especially in metastatic colorectal cancer, owing to the clinical inability to identify dormant cells prior to their overt recurrence. Lacking clinical insights, in vitro modeling for mechanistic and therapeutic discovery is hindered. Here, we review models and methods of inducing colorectal cancer dormancy with the goal of consolidating findings for reference. We also highlight the need for advanced, tissue-engineered models to better mimic the organ-specific 3D microenvironment of metastatic colorectal cancer. New models would enable breakthroughs in understanding mechanisms driving dormancy progression and reversal, thereby providing context for therapeutic advances to improve patient survival.
    Keywords:  colorectal cancer; dormancy; in vitro; models; tissue engineering
    DOI:  https://doi.org/10.1089/ten.teb.2025.0009
  8. Transl Oncol. 2025 Apr 03. pii: S1936-5233(25)00110-X. [Epub ahead of print]55 102379
      Colorectal peritoneal metastases (CPM) are the third most common site of metastatic spread of colorectal cancer and are associated with worse survival than other sites of metastatic disease. In recent years tumoral circulating tumoral DNA (ctDNA) mutational status has been increasingly utilized in clinical decision making for metastatic colorectal cancer patients despite its utility in CPM being poorly understood. Here we describe standard of care performed mutational profiles and associated outcomes for unresectable CPM patients, with a contextual comparison to 160 unresected colorectal liver metastases (CLM) patients. Of 508 patients, 288 (57 %) had CPM alone and 220 (43 %) had CPM with extraperitoneal metastases. Patients with synchronous CPM and CLM had worse overall survival (HR 1.67 [95 %CI 1.26-2.22]). Mutations in ctDNA were noted in 110/145 (75.9 %) of CPM patients, with mutations in KRAS or PIK3CA ctDNA being associated with worse survival. Importantly, the association between tumoral mutational profile and survival differed by site of metastatic disease. The prognostic significance of specific mutations, particularly BRAF and KRAS, differs between patients with CPM and CLM, and supports the distinct biology of these metastatic sites and the importance of tissue and circulating genomic profiling to risk-stratify these patients according to site of metastasis.
    Keywords:  BRAF mutation; Circulating tumoral DNA; Colorectal cancer; KRAS mutation; Liver metastasis; Peritoneal metastasis
    DOI:  https://doi.org/10.1016/j.tranon.2025.102379
  9. Res Sq. 2025 Mar 25. pii: rs.3.rs-6222474. [Epub ahead of print]
      Intestinal homeostasis relies on a protective mucus layer that separates bacteria from the host, with Muc2 as its primary component. This secreted, gel-forming mucin is heavily O-glycosylated, allowing it to retain water and support beneficial bacteria. For the first time, we demonstrate that Muc2 N-glycosylation plays a critical in mucin maturation, O-glycosylation, barrier integrity, and the prevention of dysbiosis. Using mouse models with global and intestine-specific N-glycan deficiency- caused by the loss of the mannose producing enzyme, Mpi- we uncover an unexpected link between N-glycosylation and intestinal homeostasis. Our findings reveal that Mpi hypomorphic mice are highly sensitive to DSS-induced colitis, while Mpiflox; VillinCre mice spontaneously develop disease, exhibiting increased ER stress and dysbiosis. Additionally, electron microscopy, proteomics, and gene expression analyses of goblet and Paneth cells indicate immaturity, mitochondrial loss, and disruptions in lipid metabolism. These results highlight the fundamental role of N-glycosylation in maintaining intestinal homeostasis.
    DOI:  https://doi.org/10.21203/rs.3.rs-6222474/v1
  10. Discov Oncol. 2025 Apr 09. 16(1): 495
       BACKGROUND: Increasing evidence suggests that resistance to 5-fluorouracil (5FU) and oxaliplatin (OXP) in colorectal cancer (CRC) is linked to poor prognosis. This study aimed to probe the effect of colony-stimulating factor 2 (CSF2) on the resistance of CRC to 5FU and OXP.
    METHODS: The expression of CSF2 in CRC and the impact of abnormal CSF2 expression on the prognosis of CRC patients were analyzed using bioinformatics. The half-maximal inhibitory concentrations (IC50) of 5FU and OXP on CRC cells were determined using the CCK-8 assay. Apoptosis in CRC cells was assessed through flow cytometry. mRNA and protein levels were measured using qRT-PCR and western blot, respectively. Gene Set Enrichment Analysis (GSEA) was conduced to investigate the signaling pathways regulated by CSF2 in CRC. The Notch pathway activator Jagged-1 (JAG) was employed to verify whether CSF2 influences the resistance of CRC cells to 5-FU and OXP by modulating the Notch signaling pathway.
    RESULTS: High expression of CSF2 is associated with poor prognosis in CRC patients. CSF2 is downregulated in CRC cells that resistance to 5-FU and OXP. Silencing CSF2 inhibits resistance to 5FU and OXP, reduces the survival of resistant CRC cells, and promotes apoptosis. CSF2 activates the Notch signaling pathway, which is highly expressed in CRC resistant cells; conversely, silencing CSF2 inhibits the activation of this pathway. Treatment with JAG reversed the effects of CSF2 silencing on resistance to 5FU and OXP in CRC cells.
    CONCLUSION: The silencing of CSF2 inhibited the resistance of CRC cells to 5FU and OXP by regulating the Notch signaling pathway.
    Keywords:  CSF2; Colorectal cancer; Notch pathway; Resistance
    DOI:  https://doi.org/10.1007/s12672-025-02285-w
  11. Cell Death Dis. 2025 Apr 05. 16(1): 255
      Trifluridine/Tipiracil (FTD/TPI, TAS102) has been approved for the treatment of patients with colorectal cancer (CRC) for its promising anticancer activity enabled by its incorporation into double strands during DNA synthesis. However, the mechanisms underlying the anticancer targets of FTD/TPI remain not fully understood. Here we report our observation of the activation of ferroptosis in CRC by FTD/TPI. Mechanistically, FTD/TPI directly promotes the ubiquitination and degradation of MDM2, thereby stabilizing the p53. Nuclear accumulation of p53 subsequently downregulates SLC7A11 expression, leading to ferroptosis. Furthermore, we observed that FTD/TPI combined with sulfasalazine (SAS), a system Xc- inhibitor, works in a synergistic manner to induce ferroptosis and further inhibit the proliferation of CRC cells. Finally, we confirmed the synergistic effect of SAS and FTD/TPI on patient-derived organoids in vitro and patient-derived xenograft mouse models in vivo. Our findings are the first to reveal that FTD/TPI induces ferroptosis via the p53-SLC7A11 axis and that SAS enhances the sensitivity and therapeutic effect of FTD/TPI. These findings suggest that the synergistic effect of FTD/TPI and SAS may represent a new therapeutic strategy for patients with CRC.
    DOI:  https://doi.org/10.1038/s41419-025-07541-z
  12. Cell Rep Med. 2025 Apr 02. pii: S2666-3791(25)00126-0. [Epub ahead of print] 102053
      Application of machine learning (ML) on cancer-specific pharmacogenomic datasets shows immense promise for identifying predictive response biomarkers to enable personalized treatment. We introduce CAN-Scan, a precision oncology platform, which applies ML on next-generation pharmacogenomic datasets generated from a freeze-viable biobank of patient-derived primary cell lines (PDCs). These PDCs are screened against 84 Food and Drug Administration (FDA)-approved drugs at clinically relevant doses (Cmax), focusing on colorectal cancer (CRC) as a model system. CAN-Scan uncovers prognostic biomarkers and alternative treatment strategies, particularly for patients unresponsive to first-line chemotherapy. Specifically, it identifies gene expression signatures linked to resistance against 5-fluorouracil (5-FU)-based drugs and a focal copy-number gain on chromosome 7q, harboring critical resistance-associated genes. CAN-Scan-derived response signatures accurately predict clinical outcomes across four independent, ethnically diverse CRC cohorts. Notably, drug-specific ML models reveal regorafenib and vemurafenib as alternative treatments for BRAF-expressing, 5-FU-insensitive CRC. Altogether, this approach demonstrates significant potential in improving biomarker discovery and guiding personalized treatments.
    Keywords:  5-FU resistance; PDC; biomarker; chromosome 7 amplification; colorectal cancer; drug screen; head and neck cancer; machine learning; patient-derived cancer models; pharmacogenomics; precision oncology
    DOI:  https://doi.org/10.1016/j.xcrm.2025.102053
  13. Nat Commun. 2025 Apr 05. 16(1): 3261
      Colorectal carcinoma (CRC) exhibits metastatic organotropism, primarily targeting liver, lung, and rarely the brain. Here, we study chromosomal imbalances (CIs) in cohorts of primary CRCs and metastases. Brain metastases show the highest burden of CIs, including aneuploidies and focal CIs, with enrichment of +12p encoding KRAS. Compared to liver and lung metastases, brain metastases present with increased co-occurrence of KRAS mutation and amplification. CRCs with concurrent KRAS mutation and amplification display significant metabolic reprogramming with upregulation of glycolysis, alongside upregulation of cell cycle pathways, including copy number gains of MDM2 and CDK4. Evolutionary modeling suggests early acquisition of many organotropic CIs enriched in both liver and brain metastases, while brain-enriched CIs preferentially emerge later. Collectively, this study supports a model where cytogenetic events in CRCs favor site-specific metastatic colonization. These site-enriched CI patterns may serve as biomarkers for metastatic potential in precision oncology.
    DOI:  https://doi.org/10.1038/s41467-025-58413-1