ArticleCytotechnology2023
Hypoxia-induced the upregulation of NDUFA4L2 promoted colon adenocarcinoma progression through ROS-mediated PI3K/AKT pathway.
Article in Cytotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Adaptation of OXPHOS biogenesis to cellular requirements.Protein science : a publication of the Protein Society · 2026Review
- Integrating weighted gene co-expression network analysis and machine learning reveal that NDUFA4L2 alleviates KA-induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction.Journal of bioenergetics and biomembranes · 2026Article
- NDUFA4L2 regulates the progression and chemotherapy sensitivity of HNSCC by inhibiting PANoptosis.NPJ precision oncology · 2026Article
- Nucleotide metabolism-associated drug resistance gene NDUFA4L2 promotes colon cancer progression and 5-FU resistance.Scientific reports · 2025Article
- Serum metabolomics-based diagnostic biomarkers for colorectal cancer: insights and multi-omics validation.Frontiers in endocrinology · 2025Article
- Constructing a novel mitochondrial metabolism-related genes signature to evaluate tumor immune microenvironment and predict survival of colorectal cancer.Frontiers in medicine · 2025Article
- Pancancer analysis of NDUFA4L2 with focused role in tumor progression and metastasis of colon adenocarcinoma.Medical oncology (Northwood, London, England) · 2024Article
- DKK2 promotes the progression of oral squamous cell carcinoma through the PI3K/AKT signaling pathway.Aging · 2024Article
- Exploring the metastasis-related biomarker and carcinogenic mechanism in liver cancer based on single cell technology.Heliyon · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 4-like 2 (NDUFA4L2) gene has been reported to be upregulated in colorectal cancer (CRC) and is associated with worse prognosis. However, the specific function and underlying mechanism of NDUFA4L2 in colon adenocarcinoma (COAD) under hypoxia has never been investigated. Our study discovered that hypoxia promoted the viability, metastasis, and epithelial-mesenchymal transition (EMT) of COAD cells. Besides, hypoxia-induced HIF-1α upregulated the expression of NDUFA4L2 which served as an oncogene and an independent diagnostic and prognostic marker in COAD. Under hypoxic environment, NDUFA4L2 mediated the viability, metastasis, and epithelial-EMT of COAD cells. Additionally, the ROS-dependent PI3K/Akt signaling was activated by NDUFA4L2 in COAD in hypoxia and NDUFA4L2 facilitated the malignant behaviors of hypoxia-treated COAD cells by elevating ROS production. Collectively, abundant NDUFA4L2 expression induced by HIF-1α under hypoxia promoted the development of COAD through activation of the PI3K/AKT signaling in a ROS-dependent manner, indicating NDUFA4L2 as a promising target in COAD diagnosis and treatment.
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