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PubMed2025

PKCζ, CTNNBIP1 and ALDH1A3 Expression in Luminal B Breast Cancer Indicates Decreased Hormone Therapy Effectiveness.

BACKGROUND/AIM: The role of catenin β interacting protein 1 (CTNNBIP1), a negative regulator of the canonical Wnt/β-catenin signaling pathway, in luminal A and B breast cancer stem cells treated with hormone therapy is unknown. This study investigated the relationship between CTNNBIP1 and aldehyde dehydrogenase 1 family member A3 (ALDH1A3) expression and its impact on disease-specific survival in luminal A and B breast cancer. Given that high protein kinase ζ (PKCζ) expression, together with elevated CTNNBIP1 or ALDH1A3, is linked to poor prognosis in luminal B tumors, we also examined their combined influence. MATERIALS AND METHODS: Gene expression and clinical data from the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC; n=2,509) were analyzed using Kaplan-Meier and Cox proportional hazards models. Findings were validated with The Cancer Genome Atlas Pan-Cancer Atlas (TCGA; n=1,084). RESULTS: CTNNBIP1 high ALDH1A3 high indicated a poor prognosis in patients with luminal B breast cancer treated with hormone therapy in the METABRIC dataset and aromatase inhibitors as hormone therapy in the TCGA data set, suggesting that high CTNNBIP1 and ALDH1A3 expression contributed to decreased effectiveness of hormone therapy in patients with luminal B breast cancer. PKC ζ high CTNNBIP1 high ALDH1A3 high was associated with a poor prognosis in patients with luminal B breast cancer treated with hormone therapy and aromatase inhibitors, suggesting that high PKC ζ , CTNNBIP1 and ALDH1A3 expression contributed to decreased effectiveness of hormone therapy in patients with luminal B breast cancer. CONCLUSION: PKC ζ and CTNNBIP1 may be involved in the progression of ALDH1A3-positive luminal B breast cancer. In luminal B breast cancer, PKC ζ , CTNNBIP1 and ALDH1A3 could serve as molecular drug targets and prognostic biomarkers to predict the effectiveness of hormone therapy.

ALDH1A3↗
PubMed2025

High p62 and ALDH1A3 Reduce the Effectiveness of Endocrine Therapy in Luminal B Breast Cancer.

BACKGROUND/AIM: High expression of p62 and ALDH1A3 indicates a poor clinical outcome in luminal B breast cancer, and p62 is involved in the progression of ALDH1-positive luminal B breast cancer stem cells. However, the association between endocrine therapy and high p62 and ALDH1A3 expression, in luminal B breast cancer remains unclear. MATERIALS AND METHODS: Two datasets with gene expression and clinical data for patients with primary breast cancer (METABRIC, n=2,509; The Cancer Genome Atlas, n=1,084) were downloaded and statistically analyzed. To evaluate the association between the p62 and ALDH1A3 expression levels and endocrine therapy, including tamoxifen and aromatase inhibitor, in patients with luminal B breast cancer, disease-specific survival was examined using Kaplan-Meier and multivariate Cox regression analyses. RESULTS: Patients with p62 high ALDH1A3 high luminal B breast cancer treated with endocrine therapy exhibited a poor prognosis. Moreover, patients with p62 high ALDH1A3 high luminal B breast cancer treated with tamoxifen showed a trend towards a poor prognosis, but those treated with aromatase inhibitors showed a significantly poor prognosis. These results suggest that endocrine therapy, especially aromatase inhibitors, exhibits a reduced effectiveness against p62 high ALDH1A3 high luminal B tumors. CONCLUSION: p62 and ALDH1A3 could be used together as a prognostic biomarker for predicting the efficacy of endocrine therapy for luminal B breast cancer.

ALDH1A3↗
PubMed2026

A retinoic acid autoregulatory loop governing prefrontal-motor arealization.

The frontal lobe comprises the prefrontal association cortex (PFC), which supports complex cognition and goal-directed behaviour, and the motor cortex (MC), which executes movement1-14. The establishment of distinct regional identities and connections along the sensorimotor-to-association axis provides a fundamental scaffold for cortical areal organization and function15-19. Retinoic acid (RA) signalling has emerged as a key regulator of PFC development19-26. However, the mechanisms that spatially confine RA signalling within the developing PFC, and the downstream RA-responsive gene networks, remain poorly understood. Here we define an RA-associated gene regulatory network in the developing human PFC and identify MEIS2, which encodes a transcription factor linked to intellectual disability and autism spectrum disorder, as a key hub of this network. Conditional deletion of Meis2 in postmitotic cortical excitatory neurons in mice results in a partial respecification of prospective prefrontal association territories towards motor-like molecular and connectivity features, highlighting a critical role of postmitotic neurons in establishing and maintaining cortical areal identities. Concomitant with Meis2 loss, the population of excitatory neurons expressing the RA-synthesizing enzyme ALDH1A3, and consequently RA signalling itself, is substantially reduced in the developing medial PFC (mPFC). These findings reveal a conserved autoregulatory loop, RA → MEIS2 → ALDH1A3 → RA, that reinforces a PFC-enriched RA gradient and organizes the MC-PFC axis. Together, our findings reveal a postmitotic mechanism by which specific features of neuronal identity reinforce RA signalling to define key features of prefrontal and motor cortical territories, linking a classic morphogen to transcriptional identity, neural circuit formation and function, and potentially to neuropsychiatric disorders.

Journal Article↗
PubMed2026

Host eicosanoid signals define a granuloma fibroblast population that coordinates mycobacterial containment.

Genetic variation at the leukotriene A4 hydrolase (LTA4H) locus is associated with tuberculosis (TB) severity and outcome. Here, we define a unique population of peripheral fibroblasts at the mycobacterial granuloma, the central immune structure in TB, whose recruitment and functions are coordinated by lta4h-dependent signals. Using single-cell profiling of zebrafish mycobacterial infections, we identify a layer of lta4h-dependent recruited fibroblasts at the granuloma's edge with mesenchymal and stem-like expression signatures, including aldh1a3 expression. Ablation of these cells compromises bacterial containment at the structure's periphery. Similarly, genetic disruption of apolipoprotein D, produced specifically in granuloma-associated fibroblasts, results in an altered eicosanoid balance, decreased inflammation, and increased dissemination of infection. In humans, this granuloma-associated fibroblast population is distinct from myofibroblasts, interacts with LTA4H-expressing macrophages, and is prominent across diverse TB granuloma types. These results link a host genetic susceptibility locus to the recruitment and function of a specialized fibroblast population that limits bacterial dissemination.

Animals↗
PubMed2026

Spatial Mapping of the Precancer-to-Cancer Transition in Breast and Prostate.

UNLABELLED: Breast and prostate cancers are both hormone-driven adenocarcinomas that undergo analogous invasion programs. Using lightsheet microscopy on intact tumors, we identified transitional junctions between precancerous and invasive regions. We then developed a multimodal serial-section workflow integrating volumetric reconstruction with spatial transcriptomics. Analysis of 319 spatial assays from 51 cases revealed gene expression features and novel structural insights defining the shift from precancer to invasive disease. In breast cancer, loss of MGP and PLAT was associated with invasive transition and promoted tumorigenesis in functional assays. In prostate cancer, GDF15, ALDH1A3, ANPEP, and FASN were upregulated along invasive progression, and their knockdown in PC-3 cells suppressed proliferation and migration. Enrichment of tumor-associated macrophages (SPP1+ and MS4A6A+) along non-triple-negative breast cancer breast cancer transitions highlights immune involvement as a potential driver of invasiveness. SIGNIFICANCE: Our method of defining precise spatial locations of invasive transition allows for the direct interrogation of transition drivers, presenting new therapeutic targets for the two most prevalent cancers and providing a framework for studying spatially defined mechanisms of tumor progression. See related commentary by Jing and Li, p. 1720.

Humans↗