ArticleCancer genomics & proteomics
NRF1 Activates the AMPK/SIRT1/PGC-1α/TFAM Axis to Suppress EMT and Tumor Progression in Lung Adenocarcinoma.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
aimLung cancer is the leading cause of cancer-related mortality globally, emphasizing the need for identifying molecular mechanisms that drive its progression and therapeutic resistance. Nuclear respiratory factor 1 (NRF1) is a transcription factor involved in mitochondrial biogenesis, apoptosis, and epithelial-mesenchymal transition (EMT), all of which contribute to cancer initiation and metastasis. This study investigated the role of NRF1 in lung cancer progression and its potential as a therapeutic target. MATERIALS AND
methodsA549 lung adenocarcinoma cells were used to evaluate the effects of NRF1 overexpression (pcDNA-NRF1) and silencing (shRNA-NRF1). Moreover, western blotting were used to assess EMT markers (E-cadherin, N-cadherin, vimentin), mitochondrial biogenesis factors (T-fam), and apoptotic markers (caspase-3, caspase-9). Functional assays were performed to measure cell migration, and apoptosis. SCID mice implanted with NRF1-modified tumors were used for
resultsNRF1 overexpression increased E-cadherin while reducing N-cadherin and vimentin, inhibiting EMT. It suppressed cell migration while enhancing mitochondrial biogenesis and apoptosis, as indicated by elevated caspase-3 and caspase-9 activity. Conversely, NRF1 silencing promoted EMT, reduced mitochondrial biogenesis, and decreased apoptosis.
conclusionNRF1 acts as a suppressor of EMT and a promoter of mitochondrial biogenesis and apoptosis in lung cancer. Its regulatory role suggests NRF1 as a potential therapeutic target for inhibiting tumor progression and overcoming resistance to conventional therapies.
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