bims-instec Biomed News
on Intestinal stem cells and chemoresistance in colon cancer and intestinal regeneration
Issue of 2025–03–23
eleven papers selected by
Maria-Virginia Giolito, Université Catholique de Louvain



  1. Cell Chem Biol. 2025 Mar 20. pii: S2451-9456(25)00065-0. [Epub ahead of print]32(3): 389-391
      Differentiated progenitors in intestinal crypts react to stem cell attrition by reverting to the multipotent state. In the February issue of Nature Cell Biology, Pashos et al.1 reveal a role for H3K36 methylation at cell-type-restricted genes in helping maintain differentiated cell states, hence regulating cell plasticity and regenerative responses.
    DOI:  https://doi.org/10.1016/j.chembiol.2025.02.007
  2. J Gastrointest Oncol. 2025 Feb 28. 16(1): 292-300
       Background: Anti-epidermal growth factor receptor (EGFR) therapies are important targeted agents in the treatment of metastatic colorectal cancer (CRC). However, clinical benefit is limited to patients with left-sided primary tumors and RAS wild-type (WT) disease. In right-sided chemo-refractory settings, response to anti-EGFR therapy has not been reported to date.
    Case Description: We present a case of a 70-year-old man with metachronous metastatic ascending colon adenocarcinoma who experienced an exceptional response to FOLFIRI (fluorouracil, leucovorin, and irinotecan) plus panitumumab after failing multiple lines of therapy. He was initially diagnosed with stage IIIB (pT4aN1M0) disease and underwent hemicolectomy followed by adjuvant FOLFOX (fluorouracil, leucovorin, and oxaliplatin). Nine months after completion of adjuvant therapy, disease recurred in the liver, peritoneum, and mesenteric lymph nodes. Subsequent treatments included FOLFIRI plus bevacizumab and FOLFOX with eventual progression. Tumor genomic profiling revealed RAS/RAF WT disease, and in the absence of anti-EGFR therapy resistance mutations, the patient was offered treatment with FOLFIRI plus panitumumab. He achieved immediate palliation of his abdominal pain after one cycle, followed by normalization of his tumor markers and significant tumor regression of his hepatic, peritoneal, lung, and distant lymph node metastases within four cycles.
    Conclusions: Treatment options for right-sided RAS-WT metastatic CRC are limited, particularly after progression on standard chemotherapies. While anti-EGFR antibodies have demonstrated detrimental survival impact in the first-line setting for right-sided CRC, their performance in later lines is less well-characterized. This case challenges the notion of right-sided disease as uniformly resistant to EGFR inhibition and highlights the need for additional biomarker studies to identify the subset of right-sided CRC that may benefit from EGFR targeted strategies. Emerging evidence suggests that more stringent genomic criteria for EGFR resistance, beyond RAS mutation status alone, may refine patient selection for benefit from anti-EGFR therapies.
    Keywords:  Colorectal cancer (CRC); RAS wildtype; case report; epidermal growth factor receptor therapy (EGFR therapy); right-sided tumor
    DOI:  https://doi.org/10.21037/jgo-24-458
  3. Cell Death Dis. 2025 Mar 20. 16(1): 193
      Colorectal cancer stem cells (CCSCs) play a critical role in mediating chemoresistance. Lactylation is a post-translational modification induced by lactate that regulates gene expression. However, whether lactylation affects the chemoresistance of CCSCs remains unknown. Here, we demonstrate that histone lactylation enhances CCSC chemoresistance both in vitro and in vivo. Furthermore, our findings showed that p300 catalyzes the lactylation of histone H4 at K12, whereas HDAC1 facilitates its delactylation in CCSCs. Notably, lactylation at H4K12 (H4K12la) upregulates GCLC expression and inhibits ferroptosis in CCSCs, and the inhibition of p300 or LDHA decreases H4K12la levels, thereby increasing the chemosensitivity of CCSCs. Additionally, the GCLC inhibitor BSO promotes ferroptosis and sensitizes CCSCs to oxaliplatin. Taken together, these findings suggest that histone lactylation upregulates GCLC to inhibit ferroptosis signaling, thus enhancing CCSC chemoresistance. These findings provide new insights into the relationship between cellular metabolism and chemoresistance and suggest potential therapeutic strategies targeting p300, LDHA, and GCLC. We showed that histones H4K12 lactylation promoted chemoresistance in CSCs. p300 catalyzes the lactylation of histone H4 at K12, HDAC1 inhibits the histone lactylation at the same site. H4K12la in CSCs regulates the expression of the ferroptosis-related gene GCLC, thereby inhibiting ferroptosis and leading to chemoresistance. Targeting the p300, LDHA, or GCLC may be overcome tumor chemoresistance.
    DOI:  https://doi.org/10.1038/s41419-025-07498-z
  4. FASEB J. 2025 Mar 31. 39(6): e70474
      Emerging evidence shows that extracellular vesicles (EVs)-mediated cargo shuttling between different kinds of cells constantly occurs in the tumor microenvironment, leading to the progression of a variety of cancers, but the biological role of DNA enriched in EVs has not been fully elucidated. Here, nuclear chromatin-originated DNA fragments were identified in human serum-derived EVs and exhibited a mild increase in the colorectal cancer patient group, unveiling their potential as a biomarker for cancer diagnosis. Molecular experiments showed that chromatin and mitochondrial DNA fragments adhered to the outer membrane of EVs were released from colorectal cancer cells and transported into macrophages where they stimulated STING signaling cascades, resulting in enhanced STAT1 phosphorylation and IL6 production. Further experiments revealed that STAT1 functioned as a potential IL6 transcription regulator through directly locating at its promoter regions to facilitate IL6 expression in macrophages. In the tumor microenvironment, the accumulated IL6 released by macrophages, in turn, provoked colorectal cancer cell epithelial to mesenchymal transition (EMT) through activating IL6R/STAT3 signaling. Our findings highlighted the importance of DNA carried by EVs in shaping the tumor environment and revealed their potential as a clinical diagnostic biomarker for colorectal cancer.
    Keywords:  EMT; colorectal cancer; extracellular vesicles; macrophage
    DOI:  https://doi.org/10.1096/fj.202402757RR
  5. Pathol Res Pract. 2025 Mar 10. pii: S0344-0338(25)00101-3. [Epub ahead of print]269 155909
       BACKGROUND: Cell migration-inducing and hyaluronan-binding protein (CEMIP) is found to act as an oncogene in colorectal cancer (CRC) progression, but the underlying molecular mechanisms need to be further elucidated.
    METHODS: The mRNA and protein levels of CEMIP and membrane-associated ring-CH-type finger 8 (MARCH8) were examined by qRT-PCR and western blot. Cell functions were detected by CCK8 assay, colony formation assay and transwell assay. The levels of ROS, Fe2 +, GSH, and MDA were examined to evaluate cell ferroptosis. The interaction between MARCH8 and CEMIP was assessed by Co-IP assay and ubiquitination assay. The protein levels of ferroptosis-related markers (ACSL4, GPX4 and FTH1) and PI3K/AKT-related markers were tested using western bolt. The anti-tumor effect of MARCH8 was further confirmed by constructing xenograft tumor models.
    RESULTS: CEMIP expression was higher in CRC tissues and cells. CEMIP knockdown could suppress CRC cell proliferation, migration, invasion, and enhance ferroptosis. MARCH8 ubiquitinated CEMIP to decrease its expression, thus inhibiting CRC cell proliferation, metastasis and inducing ferroptosis. And CEMIP overexpression could abolish the anti-proliferation, anti-metastasis and pro-ferroptosis effect of MARCH8. Also, MARCH8 overexpression repressed the activity of PI3K/AKT pathway, and CEMIP upregulation partially reversed this effect. In vivo experiments suggested that MARCH8 reduced CRC tumorigenesis by inducing ferroptosis.
    CONCLUSION: MARCH8 promoted CRC cell ferroptosis via inhibiting PI3K/AKT pathway by enhancing the ubiquitination and degradation of CEMIP.
    Keywords:  CEMIP; Colorectal Cancer; Ferroptosis; MARCH8; PI3K/AKT
    DOI:  https://doi.org/10.1016/j.prp.2025.155909
  6. Cancer Lett. 2025 Mar 14. pii: S0304-3835(25)00197-1. [Epub ahead of print]618 217633
      The Hedgehog Signaling Pathway plays an important role in cancer development and chemotherapy resistance. However, whether the pathway functions depend on the metabolic reprogramming of cancer cells has not been well studied. In this study, we found that the expression level of Gli1, a key transcription factor downstream of the Hedgehog Signaling Pathway, is significantly increased in patients with pancreatic cancer resistant to gemcitabine neoadjuvant chemotherapy. Through metabolomics analysis, we confirmed that Gli1 can promote the transformation of cancer cells from a glycolytic-dominated metabolic pattern to a unique metabolic pattern called "Pentose Phosphate Recycling". Transcriptome sequencing and in vitro experiments suggest that Gli1 promotes pentose phosphate recycling through transcriptional activation of key enzymes Phosphogluconate dehydrogenase (PGD) and Transketolase (TKT). The identified metabolic rerouting in oxidative and non-oxidative pentose phosphate pathway has important physiological roles in maximizing NADPH reduction and nucleotide synthesis. Therefore, the pentose phosphate cycle driven by Gli1 can resist gemcitabine-induced DNA damage by promoting pyrimidine synthesis and resist gemcitabine-induced ferroptosis by scavenging lipid Reactive Oxygen Species (Lipid ROS). Combining the Gli1 inhibitor GANT21 with gemcitabine exerts a maximal tumor suppressor effect by simultaneously promoting DNA damage and ferroptosis. Collectively, these results reveal that Gli1 drives chemotherapy resistance in cancer cells by inducing metabolic reprogramming, providing a novel target and therapeutic strategy for reversing chemotherapy resistance.
    Keywords:  Ferroptosis; Gemcitabine resistance; Hedgehog/GLI signaling pathway; Pancreatic ductal adenocarcinoma; Pentose phosphates recycling
    DOI:  https://doi.org/10.1016/j.canlet.2025.217633
  7. Cancer Immunol Immunother. 2025 Mar 19. 74(5): 154
      BRAF-mutated colorectal cancer correlates with poor prognosis and limited response to standard treatments. Combining immune checkpoint inhibitors with BRAF/MEK inhibitors shows promise against BRAF-mutant melanoma in both preclinical and clinical trials. Therefore, we hypothesized that the treatment would be effective against BRAF-mutant colorectal cancer. In this study, we assessed the efficacy of combining immune checkpoint inhibitors with BRAF and/or MEK inhibitors in BRAF-mutant colorectal cancers. We treated BRAF V600E colorectal cancer cells HT-29 and SNU-1235 with encorafenib (BRAF inhibitor) and binimetinib (MEK inhibitor) and assessed the degrees of MAPK inhibition, JAK/STAT inhibition, cell viability, apoptosis, and the expression of antigen presenting machinery. We also inoculated HT-29 cells into mice and treated them with an immune checkpoint inhibitor (durvalumab), encorafenib, and binimetinib for 4 weeks. We found that treatment with BRAF inhibitor, MEK inhibitor, or their combination led to significant tumor growth reduction, along with the MAPK and JAK/STAT pathway inhibition, antigen presenting machinery induction, and cytotoxic T cell activation. Our study demonstrates the potential effectiveness of combining immune checkpoint inhibitors with BRAF or MEK inhibitors for BRAF-mutated colorectal cancers.
    Keywords:  Anti-PD-L1; BRAF V600E; BRAF inhibitor; Immunotherapy; MEK inhibitor
    DOI:  https://doi.org/10.1007/s00262-025-04005-3
  8. Oncogene. 2025 Mar 16.
      Chemoresistance poses a significant challenge in colorectal cancer (CRC) treatment. However, the mechanisms underlying chemoresistance remain unclear. CBX3 promoted proliferation and metastasis in CRC. However, the role and mechanism of CBX3 in chemoresistance remain unknown. Therefore, we aimed to investigate the effects and mechanisms of CBX3 on multidrug resistance in CRC. Our studies showed that higher levels of CBX3 expression were associated with poor survival, especially in groups with progression following chemotherapy. CBX3 overexpression increased Irinotecan and Oxaliplatin resistance, whereas CBX3 knockdown suppressed multidrug resistance in CRC cells. Additionally, CBX3 inhibited ferroptosis associated with multidrug resistance, and the ferroptosis activators prevented CBX3 overexpression-mediated cell survival. RNA sequencing revealed that the NRF2-signaling pathway was involved in this process. CBX3-upregulated NRF2 protein expression by directly binding to the promoter of Cullin3 (CUL3) to suppress CUL3 transcription and CUL3-mediated NRF2 degradation. Moreover, Glutathione Peroxidase 2 (GPX2) was downstream of the CBX3-NRF2 pathway in CRC chemoresistance. ML385, an NRF2 inhibitor, suppressed GPX2 expression, and increased ferroptosis in PDX models. Our study identified CBX3/NRF2/GPX2 axis may be a novel signaling pathway that mediates multidrug resistance in CRC. This study proposes developing novel strategies for cancer treatment to overcome drug resistance in the future.
    DOI:  https://doi.org/10.1038/s41388-025-03337-9
  9. Cell Chem Biol. 2025 Mar 20. pii: S2451-9456(25)00066-2. [Epub ahead of print]32(3): 384-385
      Polyunsaturated fats promote ferroptosis through their propensity to form toxic lipid peroxides. In this issue of Cell Chemical Biology, Sokol et al.1 report that extracellular lipid depletion leads to increased cell death by ferroptosis. This occurs because fats liberated from triglycerides are modified and incorporated into cellular phospholipids.
    DOI:  https://doi.org/10.1016/j.chembiol.2025.02.008
  10. Annu Rev Biochem. 2025 Mar 17.
      Metabolism and gene regulation are vital processes that need to be tightly coordinated to maintain homeostasis or to enable growth and development. Recent research has begun to reveal the surprisingly interlaced relationship between metabolism and gene expression control. Because key metabolites are cofactors or cosubstrates of chromatin-modifying enzymes, changes in their concentrations can modulate chromatin states and gene expression. Additionally, an increasing number of key metabolic enzymes are found to directly regulate chromatin and transcription in response to changes in metabolic state. These include enzymes that fuel chromatin-associated metabolism and moonlighting enzymes that function as transcription factors, independent of their enzymatic activity. Conversely, accumulating evidence suggests that chromatin itself serves key metabolic functions, independent of transcriptional regulation. Here, we discuss the bidirectional interface between metabolism and chromatin and its corruption in cancer cells.
    DOI:  https://doi.org/10.1146/annurev-biochem-030122-044718
  11. Cell Rep. 2025 Mar 13. pii: S2211-1247(25)00203-7. [Epub ahead of print]44(3): 115432
      Cancer-associated fibroblasts (CAFs) and immune cells make up two major components of the tumor microenvironment (TME), contributing to an ecosystem that can either support or restrain cancer progression. Metabolism is a key regulator of the TME, providing a means for cells to communicate with and influence each other, modulating tumor progression and anti-tumor immunity. Cells of the TME can metabolically interact directly through metabolite secretion and consumption or by influencing other aspects of the TME that, in turn, stimulate metabolic rewiring in target cells. Recent advances in understanding the subtypes and plasticity of cells in the TME both open up new avenues and create challenges for metabolically targeting the TME to hamper tumor growth and improve response to therapy. This perspective explores ways in which the CAF and immune components of the TME could metabolically influence each other, based on current knowledge of their metabolic states, interactions, and subpopulations.
    Keywords:  CAFs; CP: Cancer; CP: Metabolism; immune cells; metabolism; stroma immune; tumor microenvironment
    DOI:  https://doi.org/10.1016/j.celrep.2025.115432