bims-merabr Biomed News
on Metabolic rewiring in aggressive breast cancer
Issue of 2025–07–06
twelve papers selected by
Barbara Mensah Sankofi, University of Oklahoma Health Sciences Center
  1. Adipocytes-induced ANGPTL4/KLF4 axis drives glycolysis and metastasis in triple-negative breast cancer.
  2. SREBP-1 in obesity-induced breast cancer: mechanisms and therapeutic perspectives.
  3. NASP Promotes Triple-negative Breast Cancer Progression and Metastasis by Stabilizing YAP in a USP15-Dependent Way.
  4. Amino acid transporter LAT1 (SLC7A5) promotes metabolic rewiring in TNBC progression through the L-Trp/QPRT/NAD+ pathway.
  5. Tumor-Associated Neutrophils Regulate Breast Cancer Progression Through the AQP9/STAT3 Signaling Pathway.
  6. PRDX6 Drives Breast Cancer Progression Through Mitochondrial Biosynthesis and Oxidative Phosphorylation.
  7. Adipocyte-specific Zeb1 downregulation remodels the tumor-associated adipose microenvironment to facilitate female breast cancer progression.
  8. LINC01235 is an Upstream Regulator of the NFIB Gene and the NOTCH Pathway in Triple Negative Breast Cancer.
  9. Lipid metabolism in cancer stem cells: reprogramming, mechanisms, crosstalk, and therapeutic approaches.
  10. Age-related and postmenopausal breast cancer progression and treatment management: The significance of pro-inflammatory cytokines and CXC chemokines.
  11. Understanding the role of obesity in endocrine therapy for postmenopausal breast cancer: significance of the BIG 1-98 and ATAC trial data.
  12. SIAH2-AS1 stimulates breast cancer cell proliferation and migration via the Wnt/β-catenin signaling pathway.
  1. J Exp Clin Cancer Res. 2025 Jul 04. 44(1): 192
    Adipocytes-induced ANGPTL4/KLF4 axis drives glycolysis and metastasis in triple-negative breast cancer.
    Dou Yin, Nana Fang, Yaling Zhu, Xiaoqing Bao, Juan Yang, Qingyu Zhang, Ruimeng Wang, Jiahui Huang, Qibing Wu, Fang Ma, Xiaohui Wei.
       BACKGROUND: The adipocyte-rich tumor microenvironment (TME) is recognized as a key factor in promoting cancer progression. A distinct characteristic of peritumoral adipocytes is their reduced lipid content and the acquisition of a proinflammatory phenotype. However, the underlying mechanisms by which adipocytes rewire metabolism and boost tumor progression in triple-negative breast cancer (TNBC) remain poorly understood.
    METHODS: We utilized transcriptomic analysis, bioinformatic analysis, metabolic flux analysis, protein-protein docking, gene and protein expression profiling, in vivo metastasis analysis and breast cancer specimens to explore how adipocytes reprogram tumor metabolism and progression in TNBC.
    RESULTS: Our findings reveal that Angiopoietin-like 4 (ANGPTL4) exhibits significantly higher expression levels in adipocyte-rich tumor circumstance compared to the symbiotic environment lacking of adipocyte. Furthermore, ANGPTL4 expression in tumor cells is essential for adipocyte-driven glycolysis and metastasis. Interleukin 6 (IL-6), enriched in cancer-associated adipocytes, and lipolysis-derived free fatty acids (FFAs) released from adipocytes, amplify ANGPTL4-mediated glycolysis and metastasis through activation of STAT3 and PPARα pathways in TNBC cells. Additionally, ANGPTL4 interacts with transcription factor KLF4 and enhances KLF4 activity, which further drives glycolysis and metastasis, whereas KLF4 knockdown attenuates migration and glycolysis in TNBC cells. Importantly, Elevated ANGPTL4 and KLF4 expression was observed in metastatic breast cancer specimens compared to non-metastatic cases and was positively correlated with poor prognosis.
    CONCLUSION: Collectively, our results uncover a complex metabolic interaction between adipocytes and TNBC cells that promotes tumor aggressiveness. ANGPTL4 emerges as a key mediator in this process, making it a promising therapeutic target to inhibit TNBC progression.
    Keywords:  ANGPTL4; Adipocytes; KLF4; Lipolysis; Triple-Negative Breast Cancer
    DOI:  https://doi.org/10.1186/s13046-025-03458-9
  2. Mol Biol Rep. 2025 Jul 01. 52(1): 663
    SREBP-1 in obesity-induced breast cancer: mechanisms and therapeutic perspectives.
    Urvashi Tiwari, Salman Akhtar, Snober S Mir, Mohammad Kalim Ahmad Khan.
      Breast cancer is the most prevalent form of malignant cancer among women worldwide, and obesity is a significant risk factor. Sterol regulatory element-binding protein 1 (SREBP-1) is a crucial transcription factor that governs lipid synthesis and is aberrantly activated in obesity-induced breast cancer. This review examines the intricate relationship between SREBP-1, obesity, and breast cancer, emphasizing the mechanisms by which obesity-induced activation of SREBP-1 facilitates tumor growth, metastasis, and therapeutic resistance. Obesity disrupts the PI3K/AKT/mTOR and AMPK pathways, resulting in hyperactivation of SREBP-1 and excessive lipid accumulation in breast cancer cells. This metabolic reprogramming fosters a tumor-supportive microenvironment, thereby enhancing cancer cell proliferation, survival, and epithelial-mesenchymal transition. Moreover, obesity adversely affects various breast cancer therapies, including surgery, radiotherapy, chemotherapy, endocrine therapy, and immunotherapy by inducing drug resistance and exacerbating side effects. Targeting SREBP-1 and its regulatory pathways is a promising therapeutic strategy for obesity-induced breast cancer. Natural compounds and small molecules such as fatostatin, mollugin, xanthohumol, and docosahexaenoic acid have demonstrated potential in inhibiting SREBP-1 activation and reducing lipid synthesis in breast cancer cells. Integrating these targeted therapies with conventional treatments may enhance the outcomes of obese patients with breast cancer. Further research is warranted to elucidate the complex mechanisms linking metabolic imbalance and breast cancer, and to develop innovative strategies that effectively combine metabolic and oncological approaches.
    Keywords:  Breast cancer; Lipid synthesis; Metastasis; Obesity; SREBP-1; Therapeutic resistance
    DOI:  https://doi.org/10.1007/s11033-025-10775-x
  3. Int J Biol Sci. 2025 ;21(9): 4172-4186
    NASP Promotes Triple-negative Breast Cancer Progression and Metastasis by Stabilizing YAP in a USP15-Dependent Way.
    Wenfang Zheng, Qifeng Luo, Xuehui Wang, Xiqian Zhou, Danrong Ye, Kaiyao Hua, Lin Fang.
      Triple-negative breast cancer (TNBC) was a subtype of breast cancer with high rate of metastasis and poor prognosis. Thus, it is urgent to explore the underlying mechanism of TNBC metastasis and seek for potential therapeutic targets to improve the prognosis of TNBC patients. Here we reported that nuclear autoantigenic sperm protein (NASP) was highly expressed in TNBC and related to poor prognosis of TNBC patients. NASP acted as an oncogene that promoted the progression and metastasis of TNBC. Mechanistically, high expression of NASP in TNBC was induced by SRSF1-mediated stabilization of NASP mRNA. NASP interacted with USP15 and facilitated its activity, which resulted in the deubiquitylation and stabilization of YAP by erasing K48-linked polyubiquitination. Moreover, in vivo studies validated the role of NASP in stimulating TNBC growth and metastasis. Altogether, NASP promoted TNBC progression and metastasis by stabilizing YAP in a USP15-dependent way. It might provide new insights and potential therapeutic targets for preventing TNBC metastasis and improving the prognosis of TNBC patients.
    Keywords:  NASP; USP15; YAP; metastasis; triple-negative breast cancer
    DOI:  https://doi.org/10.7150/ijbs.99438
  4. J Exp Clin Cancer Res. 2025 Jul 03. 44(1): 190
    Amino acid transporter LAT1 (SLC7A5) promotes metabolic rewiring in TNBC progression through the L-Trp/QPRT/NAD+ pathway.
    Margot Y Fedoroff, Lei Zhao, Shaomin Wang, Alok Bhushan, Haifeng Yang, Karen M Bussard, Stephen C Peiper, Jun He.
       BACKGROUND: Cancer cells uptake excessive nutrients by expressing higher levels of glucose and/or amino acid transporters to meet their increased energy demands. L-type amino acid transporter 1 (LAT1), is regarded as a cancer-specific transporter for the uptake of large neutral amino acids such as L-tryptophan. However, the mechanism by which LAT1 rewires cellular metabolism to promote cancer progression and chemoresistance have not yet been investigated.
    METHODS: The protein levels of LAT1, p-PKM2, and p-LDHA were determined in breast cancer tissue arrays by immunohistochemistry staining followed by survival analysis. The orthotopic breast cancer models in mice, syngeneic breast cancer models, and patient-derived xenograft (PDX) mouse models were used to study the effects of LAT1 inhibition in tumor growth and chemoresistance. Steady-state polar metabolite analysis was performed to profile changes in cellular metabolism by LC-MS. The pyruvate and lactate assays as well as the seahorse assay using LAT1 knockdown cells and control cells were conducted to evaluate cellular glycolytic activities.
    RESULTS: The LAT1 protein levels were positively correlated with poor survival in triple-negative breast cancer (TNBC) patients. LAT1 silencing resulted in reduced TNBC cell viability, proliferation, migration, invasion in vitro, as well as tumor growth in vivo. The knockdown of LAT1 reduced glycolytic activities via activating PKM2 and LDHA, two key glycolytic enzymes essential for cancer cell growth. Mechanistically, we demonstrated that LAT1 promoted de novo NAD + synthesis by facilitating L-tryptophan uptake and upregulating quinolinate phosphoribosyltransferase (QPRT), the rate-limiting enzyme in this pathway. This resulted in an increased cytosolic NAD+/NADH ratio, which enhanced the phosphorylation of pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA), thus promoting TNBC tumor progression. Notably, upregulation of this pathway was observed in primary cells from doxorubicin (Dox)-resistant TNBC patient-derived xenograft (PDX) tumors and in Dox-resistant MDA-MB-231 cells. LAT1 inhibition sensitized resistant cells to Dox-induced cytotoxicity while supplementation of L-Trp/NAD + partially reversed the enhanced sensitivity to Doxorubicin induced by LAT1 knockdown. Furthermore, treatment with a LAT1-specific inhibitor JPH203 synergistically enhanced the efficacy of doxorubicin in TNBC cells.
    CONCLUSION: These findings identify a novel role of LAT1 in promoting TNBC progression and chemo-resistance by amplifying the Warburg effect, positioning LAT1 as a promising therapeutic target for TNBC treatment.
    Keywords:  Glycolysis; L-Tryptophan; LAT1 (SLC7A5); LDHA; NAD +/NADH; PKM2; QPRT; TNBC
    DOI:  https://doi.org/10.1186/s13046-025-03446-z
  5. Cancer Sci. 2025 Jun 28.
    Tumor-Associated Neutrophils Regulate Breast Cancer Progression Through the AQP9/STAT3 Signaling Pathway.
    Wuqin Xu, Guilu Zhu, Youjing Sheng, Wenjun Zhang, Shujing Wang, Qiang Wu.
      Tumor-associated neutrophils (TANs) contribute to breast cancer (BC) progression, and aquaporin 9 (AQP9) plays a critical role in tumor development. However, the interactions between TANs and AQP9 in BC are poorly understood. Bioinformatics analyses and clinical samples revealed a positive correlation between neutrophil infiltration and AQP9 expression in BC. Treating BC cells with TAN-conditioned media significantly elevated AQP9 expression compared with neutrophil-conditioned and control media treatments. Immunohistochemical analysis revealed higher AQP9 protein expression in BC tissues than in adjacent normal tissues, and AQP9 expression was negatively correlated with recurrence-free survival and overall survival in patients with BC. Functional studies demonstrated that AQP9 promoted BC cell proliferation but did not affect migration or invasion. AQP9 knockdown markedly inhibited the ability of TANs to enhance BC cell proliferation, migration, and invasion. Intravenous and intratumoral injection of TANs in mice increased tumor growth rate, weight, and volume compared with controls; moreover, histological examination revealed lung metastasis in two mice and bone involvement in one mouse out of six in the TAN treatment group. AQP9 knockdown significantly reduced the tumor growth rate. In BC cells, TAN treatment elevated STAT3 phosphorylation, and this effect was amplified by AQP9 overexpression. In conclusion, TANs promote BC progression by enhancing STAT3 phosphorylation through AQP9 upregulation. AQP9 is crucial for TAN-mediated BC progression and is a potential target for immunotherapy in patients with BC.
    Keywords:  AQP9; breast cancer; prognosis; tumor microenvironment; tumor‐associated neutrophils
    DOI:  https://doi.org/10.1111/cas.70121
  6. Cancer Med. 2025 Jul;14(13): e71005
    PRDX6 Drives Breast Cancer Progression Through Mitochondrial Biosynthesis and Oxidative Phosphorylation.
    Mei Dai, Danhua Zhang.
       BACKGROUND: Peroxiredoxin 6 (PRDX6) scavenges reactive oxygen species (ROS) and plays a key role in antioxidant defense. Although PRDX6 is involved in various cancers, its role in breast cancer (BRCA) remains unclear.
    METHODS: Cell proliferation was assessed using CCK-8, EdU staining, and colony formation assays. Migration and invasion were evaluated via wound-healing and transwell assays. ROS levels and mitochondrial membrane potential were measured by fluorescence microscopy or flow cytometry. Oxidative phosphorylation (OXPHOS) activity was determined by ATP production and NAD+/NADH ratio. Mitochondria were visualized by TEM, and mitochondrial complex subunits were detected by quantitative real-time PCR and Western blotting. In vivo effects were evaluated using a xenograft tumor model.
    RESULTS: Although PRDX6 was downregulated in BRCA overall, it showed elevated expression in aggressive subtypes and advanced-stage tumors, correlating with poor prognosis. Overexpression of PRDX6 enhanced BRCA cell proliferation, migration, and invasion. PRDX6 reduced ROS levels, upregulated mitochondrial transcription factor A (TFAM) expression, and promoted mitochondrial complex subunit expression and OXPHOS. Inhibition of TFAM led to a decrease in the expression of some of the mitochondrial complex subunits, which reversed the pro-carcinogenic phenotype of the tumor. PRDX6 also promoted tumor growth in vivo.
    CONCLUSION: PRDX6 maintains intracellular homeostasis by reducing ROS and promotes mitochondrial biogenesis and OXPHOS through TFAM-dependent and -independent pathways, driving BRCA progression.
    Keywords:  PRDX6; breast cancer; mitochondria; oxidative phosphorylation (OXPHOS); tumorigenesis
    DOI:  https://doi.org/10.1002/cam4.71005
  7. Nat Commun. 2025 Jul 01. 16(1): 6011
    Adipocyte-specific Zeb1 downregulation remodels the tumor-associated adipose microenvironment to facilitate female breast cancer progression.
    Lixia Cao, Wei Sun, Xiao Chen, Lei Liu, Shaorong Zhao, Jingjing Liu, Yang Ou, Min Guo, Chunchun Qi, Zhaoxian Li, Jie Shi, Yuxin Liu, Qiuying Shuai, Siyu Zuo, Huayu Hu, Tianwen Yu, Yanjing Wang, Mengdan Feng, Jianying Lv, Hang Wang, Peiqing Sun, Jin Zhang, Longlong Wang, Yi Shi, Shuang Yang.
      Upon penetrating the basement membrane, breast cancer cells directly interact with their surrounding adipose tissue, which forms a unique tumor-associated adipose microenvironment (TAME). However, the underlying mechanism of lipid metabolic remodeling in the TAME remains elusive. Herein, we report a Zeb1-orchestrated bidirectional communication between breast cancer cells and their adjacent cancer-associated adipocytes (CAAs). At the molecular level, breast cancer cells, through the secretion of adrenomedullin (AM), induce downregulation of Zeb1 expression to activate the Atgl/Hsl/Scd-dependent lipolysis in CAAs, resulting in the release of palmitoleic acid (POA) into the TAME. In turn, the increased POA in breast cancer competes with arachidonic acid (ARA) for the phospholipid synthesis, leaving more ARA is utilized for PDG2 production to trigger the malignant progression of breast cancer and AM production. Importantly, disruption of Zeb1-dependent lipolytic activity and/or membrane phospholipid remodeling within the TAME dramatically diminishes the aggressiveness of breast cancer in vitro and in vivo.
    DOI:  https://doi.org/10.1038/s41467-025-61088-3
  8. Mol Cancer Res. 2025 Jun 30.
    LINC01235 is an Upstream Regulator of the NFIB Gene and the NOTCH Pathway in Triple Negative Breast Cancer.
    Wenbo Xu, Sonam Bhatia, Yunus Sahin, David L Spector.
      We identified a long non-coding RNA (lncRNA), LINC01235, with significant enrichment in luminal progenitor (LP)-like cells in triple negative breast cancer organoids and cell lines. Antisense-mediated knockdown or genetic knockout of LINC01235 in TNBC cell lines led to a decline in cell proliferation and adversely impacted the ability to form organoids. A comprehensive co-expression analysis, leveraging TCGA data, revealed a distinct correlation between LINC01235 expression and the expression of NFIB, a neighboring gene encoding a transcription factor. Subsequent CRISPR knockout or ASO-mediated knockdown studies demonstrated an upstream regulatory role of LINC01235 over NFIB. Moreover, our investigations demonstrated that LINC01235 regulates the NOTCH pathway through NFIB, and ChIRP-qPCR results indicated the direct binding of LINC01235 to the NFIB promoter. Our findings demonstrate that LINC01235 positively regulates NFIB transcription, which in turn modulates the NOTCH pathway, influencing LP-like cell proliferation in breast cancer progression. This study highlights a pivotal role of LINC01235 in TNBC and its potential as a therapeutic target. Implications: This study demonstrates the central role of LINC01235 as an upstream positive regulator of NFIB and the NOTCH signaling pathway to induce the production of luminal progenitor-like cells in TNBC.
    DOI:  https://doi.org/10.1158/1541-7786.MCR-24-1143
  9. Cell Oncol (Dordr). 2025 Jun 30.
    Lipid metabolism in cancer stem cells: reprogramming, mechanisms, crosstalk, and therapeutic approaches.
    Haksoo Lee, Sujin Park, Jongwon Lee, Chaeyoung Lee, Hyunkoo Kang, JiHoon Kang, Jung Sub Lee, Eunguk Shin, HyeSook Youn, BuHyun Youn.
      Cancer stem cells (CSCs) are a highly plastic subpopulation of tumor cells with capabilities for self-renewal, therapy resistance, and metastasis. Recent evidence highlights lipid metabolic reprogramming as a central mechanism supporting these malignant traits. This review synthesizes current findings on key lipid metabolic processes in CSCs-including lipid uptake via CD36, intracellular storage in lipid droplets, de novo fatty acid synthesis by fatty acid synthase (FASN), fatty acid oxidation (FAO) regulated by carnitine palmitoyltransferase 1A (CPT1A), and cholesterol biosynthesis through the mevalonate pathway. Although many of these pathways are active in bulk cancer cells, CSCs demonstrate greater functional reliance on them, leading to enhanced survival, redox balance, and adaptation to therapy. These metabolic preferences vary by cancer type, underscoring the need for context-specific approaches. Moreover, stromal components of the tumor microenvironment (TME), such as cancer-associated fibroblasts, adipocytes, and mesenchymal stem cells, modulate CSC lipid metabolism through paracrine signals and substrate transfer, reinforcing CSC maintenance and drug resistance. Therapeutic strategies targeting lipid metabolism-such as inhibition of SCD1, CPT1A, and HMG-CoA reductase-have shown promising preclinical results in selectively depleting CSC populations and sensitizing tumors to treatment. However, challenges remain in preserving normal stem cell function, which also depends on lipid pathways. This review underscores the emerging significance of lipid metabolism as both a hallmark and vulnerability of CSCs, offering opportunities for novel targeted cancer therapies.
    Keywords:  Cancer stem cells; Chemoresistance; Lipid metabolism; Metabolic reprogramming; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s13402-025-01081-6
  10. Genes Dis. 2025 Sep;12(5): 101606
    Age-related and postmenopausal breast cancer progression and treatment management: The significance of pro-inflammatory cytokines and CXC chemokines.
    Amin Ullah, Rajeev K Singla, Dan Cao, Boyang Chen, Bairong Shen.
      Older age is one of the leading risk indicators for advanced breast cancer. It is critical to extensively investigate how aging affects breast cancer, considering the increasing rate of population aging. Human body aging and death are caused by cellular senescence and alterations in the aging microenvironment in vivo. Breast cancer cells may invade more easily with age due to the stiff extracellular matrix of the breast. Furthermore, growing evidence suggests that the massive release of inflammatory immune mediators, such as cytokines (interleukins) or CXC chemokines (CXCs), and their receptors (CXCRs), including interleukin (IL)-6, IL-8/CXCL8, tumor necrosis factor (TNF), interferon (INF), transforming growth factor (TGF), CXCL1, CXCL9, CXCL10, CXCL11/CXCR3, and CXCL12/CXCR4, plays a critical role in the development of breast cancer in elderly patients. Researchers are particularly interested in obesity-induced inflammation because it has been shown to raise the risk of breast cancer in postmenopausal women with higher body mass index. Obesity-triggered inflammation causes increased infiltration of proinflammatory cytokines, adipokines, immune cells, and tumor cells in the enlarged adipose tissue of postmenopausal women with breast cancer, thereby modulating the tumor's immune-mediated microenvironment. Therefore, in this review, we focus on the functional significance studies of proinflammatory cytokines, CXCs, and CXCRs and describe their roles in influencing breast cancer progression in older women and their factors, such as obesity in postmenopausal women. In addition, the current status and prospects of cytokine- and CXC-based theranostic interventions for breast cancer therapy in elderly and postmenopausal women are discussed.
    Keywords:  Age; Breast cancer; CXC chemokines; Obesity; Postmenopausal women; Pro-inflammatory cytokines; Theranostic strategies
    DOI:  https://doi.org/10.1016/j.gendis.2025.101606
  11. Discov Oncol. 2025 Jul 01. 16(1): 1233
    Understanding the role of obesity in endocrine therapy for postmenopausal breast cancer: significance of the BIG 1-98 and ATAC trial data.
    Sixten Harborg, Signe Borgquist.
      Obesity is a known risk factor for poor breast cancer outcomes, but its impact on endocrine therapy efficacy remains unclear. While the ATAC trial suggests reduced effectiveness of aromatase inhibitors (AIs) in women with obesity, the BIG 1-98 trial found no significant differences. Clinical and biological evidence indicates that obesity may impair AI efficacy by increasing aromatase activity and altering drug metabolism, whereas tamoxifen remains largely unaffected. Pooling data from these trials would enable detailed analyses across body composition categories, addressing discrepancies and potentially guide personalized treatment strategies. Understanding the interaction between obesity and endocrine therapy is crucial for optimizing breast cancer care.
    DOI:  https://doi.org/10.1007/s12672-025-02857-w
  12. Sci Rep. 2025 Jul 01. 15(1): 21911
    SIAH2-AS1 stimulates breast cancer cell proliferation and migration via the Wnt/β-catenin signaling pathway.
    Ying Xu, Hongmei Xiao, Zhongwen Li, Jing Li.
      Breast cancer (BC) has become a severe threat to women, which has imposed excessive pressure on society. LncRNAs play a crucial role in the occurrence and development of BC. This study aimed to evaluate the lncRNA SIAH2 antisense RNA 1 (SIAH2-AS1) role in the development and progression of BC and explore the mechanism of SIAH2-AS1 related Wnt signaling pathway in BC. Malignant and paracancer normal breast tissue samples were obtained from patients who underwent surgery at the Second Affiliated Hospital of Zunyi Medical University. Subsequently, quantitative RT-PCR (qRT-PCR) was performed with these acquired tissue samples to evaluate the concentrations of SIAH2-AS1. Furthermore, CCK-8 assays, colony formation, wound healing, and transwell were performed to investigate the cell proliferation, migration, and invasion respectively. Western blotting was eventually performed for the investigation of proteins and EMT-related markers in the Wnt/β-catenin signaling pathway. The expression of SIAH2-AS1 was up-regulated in cancer tissues and cells. Cell proliferation, colony formation, invasiveness, and migration are significantly reduced by silencing SIAH2-AS1. Moreover, E-cadherin expression in BC cells was increased, whereas N-cadherin and vimentin expression was decreased, when SIAH2-AS1 was eliminated from the cells. Additionally, the Wnt/β-catenin signaling pathways cyclin D1 and C-myc proteins were also significantly downregulated in BC cells when SIAH2-AS1 was knocked out. Our study confirms that SIAH2-AS1 activates the Wnt/β-catenin pathway and has an oncogenic activity that promotes the prognosis of BC, suggesting that SIAH2-AS1 may be a potential drug target for BC. The development of small - molecule inhibitors capable of specifically targeting SIAH2 - AS1 to target and modify the SIAH2 - AS1 gene in cancer cells may offer a novel strategy for clinical treatment. Keywords: breast cancer; cell proliferation; cell migration; Long noncoding RNA; Wnt signaling pathway.
    Keywords:  Breast cancer; Cell migration; Cell proliferation; Long noncoding RNA; Wnt signaling pathway
    DOI:  https://doi.org/10.1038/s41598-025-06808-x
This page is being maintained by Thomas Krichel. It was last updated on 2025‒07‒11 at 21:44.