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Romo1 overexpression was associated with poor response to treatment and shorter survival in advanced NSCLC patients treated with platinum-based chemotherapy. Romo1 could be a potential adverse predictive marker in this setting.
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Increased Romo1 expression was found to be associated with high lymph node ratio. Cancer invasiveness appeared to be a key reason for the poor survival related to highly expressed Romo1
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the diagnostic sensitivity and specificity of serum reactive oxygen species modulator 1 were only 41.38% and 86.21%, respectively, with the cutoff value of 27.22 ng/mL. The sensitivity and specificity of pleural fluid carcinoembryonic antigen were 69.23% and 88.00%, respectively, at the cutoff value of 3.05 ng/mL, while serum carcinoembryonic antigen were 80.77% and 72.00% at the cutoff value of 2.60 ng/mL.
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elevated in pleural effusion when lung cancer present
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The rs6060566 polymorphism of the Romo-1 gene was found to be an independent risk factor for DR in Caucasians with T2DM.
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Genetic polymorphisms of Romo1 gene were associated with significant risk of gastric cancer.
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These results demonstrate that tumor cell invasion in response to oxidative stress is associated with Romo1 expression and the NF-kappaB signaling pathway.
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Results demonstrate that expression of Romo1 is frequently upregulated in human glioblastomas and its elevation promotes malignant tumor progression by promoting cell cycle progression and by enhancing tumorigenicity
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Increased Romo1 expression in surgically resected NSCLC was found to be significantly associated with early recurrence and poor survival. Romo1 overexpression could be a potential adverse prognostic marker in this setting.
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Serum Romo1 discriminated NSCLC patients from the population without cancer with considerable sensitivity and specificity. Serum Romo1 could be a potential diagnostic biomarker for NSCLC.
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High ROMO1 expression is associated with Fanconi anemia.
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Romo1 may be a principal regulatory factor in the maintenance of constitutive NF-kappaB activation in tumor cells
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that ROS modulator protein 1 (ROMO1) links ROS and mitochondrial morphology and ultrastructure by modulating cristae remodeling and mitochondrial fusion
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data identify ROMO1 as a critical molecular switch that couples metabolic stress and mitochondrial morphology, linking mitochondrial fusion to cell survival.
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This study is the first to demonstrate that strict modulation of DKK1 expression in different cell types partially maintains cell survival via tight regulation of the ROS-producing ROMO1 and radiation resistance.
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Romo1 mediates mitochondrial reactive oxygen species production and apoptosis induced by oxidative stress in lung epithelial cells.
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A 19 amino acid peptide (pCM19) at positions 42-60 of hGlyrichin is crucial for its antibacterial activity.
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Romo1 expression induced by Myc during G1 phase stimulates Skp2-mediated Myc degradation in a negative-feedback mechanism
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increased Bcl-XL expression, which is observed in many cancer cells, confers resistance to oxidative stress in the cancer cells by suppressing Romo1-mediated oxidative stress.
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Romo1 and Bcl-X(L)) are directly associated with TNF-alpha-induced ROS production. Romo1 is a molecular bridge between TNF-alpha signaling and the mitochondria for ROS production that triggers TNF-alpha-mediated apoptosis.
