ArticleCancer cell international2022
YY1 promotes pancreatic cancer cell proliferation by enhancing mitochondrial respiration.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Transcription factor Yin Yang 1 enhances epithelial-mesenchymal transition, migration, and stemness of non-small cell lung cancer cells by targeting sonic hedgehog.Molecular and cellular biochemistry · 2025Article
- Comprehensive Analysis of Multi-Omics Data on RNA Polymerase as an Adverse Factor in Head and Neck Squamous Cell Carcinoma.Journal of inflammation research · 2025Article
- Betaine delays age-related muscle loss by mitigating Mss51-induced impairment in mitochondrial respiration via Yin Yang1.Journal of cachexia, sarcopenia and muscle · 2024Article
- Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma.European journal of histochemistry : EJH · 2024Article
- YY1 transcription factor induces proliferation and aerobic glycolysis of neuroblastoma cells via LDHA regulation.Experimental and therapeutic medicine · 2023Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
KRAS-driven metabolic reprogramming is a known peculiarity features of pancreatic ductal adenocarcinoma (PDAC) cells. However, the metabolic roles of other oncogenic genes, such as YY1, in PDAC development are still unclear. In this study, we observed significantly elevated expression of YY1 in human PDAC tissues, which positively correlated with a poor disease progression. Furthermore, in vitro studies confirmed that YY1 deletion inhibited PDAC cell proliferation and tumorigenicity. Moreover, YY1 deletion led to impaired mitochondrial RNA expression, which further inhibited mitochondrial oxidative phosphorylation (OXPHOS) complex assembly and altered cellular nucleotide homeostasis. Mechanistically, the impairment of mitochondrial OXPHOS function reduced the generation of aspartate, an output of the tricarboxylic acid cycle (TCA), and resulted in the inhibition of cell proliferation owing to unavailability of aspartate-associated nucleotides. Conversely, exogenous supplementation with aspartate fully restored PDAC cell proliferation. Our findings suggest that YY1 promotes PDAC cell proliferation by enhancing mitochondrial respiration and the TCA, which favors aspartate-associated nucleotide synthesis. Thus, targeting nucleotide biosynthesis is a promising strategy for PDAC treatment.
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