ArticleCancer science2023
Metabolic stress-induced reciprocal loop of long noncoding RNA ZFAS1 and ZEB1 promotes epithelial-mesenchymal transition and metastasis of pancreatic cancer cells.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).International journal of oncology · 2026Review
- Novel insights into lncRNAs as key regulators of post-translational modifications in cancer: mechanisms and therapeutic potential.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Targeting glutamine metabolism as a potential target for cancer treatment.Journal of experimental & clinical cancer research : CR · 2025Review
- Role of noncoding RNA and protein interaction in pancreatic cancer.Chinese medical journal · 2025Review
- The role of AMPK in pancreatic cancer: from carcinogenesis to treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Research Progress of Long Non-coding RNA-ZFAS1 in Malignant Tumors.Cell biochemistry and biophysics · 2024Review
- Progress of Exosomal LncRNAs in Pancreatic Cancer.International journal of molecular sciences · 2024Review
- A Novel AMPK Inhibitor Sensitizes Pancreatic Cancer Cells to Ferroptosis Induction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- LncRNA ZFAS1 regulates ATIC transcription and promotes the proliferation and migration of hepatocellular carcinoma through the PI3K/AKT signaling pathway.Journal of cancer research and clinical oncology · 2024Article
- Metabolic stress-induced reciprocal loop of long noncoding RNA ZFAS1 and ZEB1 promotes epithelial-mesenchymal transition and metastasis of pancreatic cancer cells.Cancer science · 2023Article
- The crosstalk among the physical tumor microenvironment and the effects of glucose deprivation on tumors in the past decade.Frontiers in cell and developmental biology · 2023Review
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Authors and funding
16 authors at 1 institution in 1 country.
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Abstract
Pancreatic cancer (PC) development faces significant metabolic stress due to metabolic reprogramming and a distinct hypovascular nature, often leading to glucose and glutamine depletion. However, the adaption mechanisms by which PC adapts to these metabolic challenges have not yet been completely explored. Here, we found that metabolic stress induced by glucose and glutamine deprivation led to an overexpression of ZNFX1 antisense RNA 1 (ZFAS1). This overexpression played a significant role in instigating PC cell epithelial-mesenchymal transition (EMT) and metastasis. Mechanistically, ZFAS1 enhanced the interaction between AMPK, a key kinase, and ZEB1, the primary regulator of EMT. This interaction resulted in the phosphorylation and subsequent stabilization of ZEB1. Interestingly, ZEB1 also reciprocally influenced the transcription of ZFAS1 by binding to its promoter. Furthermore, when ZFAS1 was depleted, the nutrient deprivation-induced EMT of PC cells and lung metastasis in nude mice were significantly inhibited. Our investigations also revealed that ZFAS1-rich exosomes released from cells suffering glucose and glutamine deprivation promoted the EMT and metastasis of recipient PC cells. Corroborating these findings, a correlated upregulation of ZFAS1 and ZEB1 expression was observed in PC tissues and was associated with a poor overall survival rate for patients. Our findings highlight the involvement of a long noncoding RNA-driven metabolic adaptation in promoting EMT and metastasis of PC, suggesting ZFAS1 as a promising novel therapeutic target for PC metabolic treatment.
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