Elevation of the Serum Apurinic/Apyrimidinic Endonuclease 1/Redox Factor-1 in Coronary Artery Disease

Jin, Seong Eun; Seo, Hee Jung; Kim, Sun Kyeong; Lee, Yu Ran; Choi, Sunga; Ahn, Kye-Taek; Kim, Jun-Hyung; Park, Jae‐Hyeong; Lee, Jae‐Hwan; Choi, Si Wan; Seong, In Whan; Jeon, Byeong Hwa; Jeong, Jin‐Ok

doi:10.4070/kcj.2015.45.5.364

Cited by 25 publications

(30 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the current study, we observed that in the tumor tissue, APE1 protein, an essential DNA repair enzyme in the BER pathway, could be a promising predictive biomarker for the responses of NSCLC patients receiving platinum-containing chemotherapy. Moreover, this previously reported nuclear protein was detected in the serum of NSCLC patients, and its level in the serum was directly correlated with the level measured in cancer tissue [12, 16, 17]. In addition, we describe herein, for the first time to our knowledge, that alteration of sAPE1 after chemotherapy is significantly associated with response and PFS of platinum-containing chemotherapy.…”

Section: Discussionsupporting

confidence: 63%

Serum APE1 as a predictive marker for platinum-based chemotherapy of non-small cell lung cancer patients

Zhang

Dai

et al. 2016

Oncotarget

View full text Add to dashboard Cite

PurposeTo define the role of the DNA repair protein apurinic/apyrimidinic endonuclease 1 (APE1) in predicting the prognosis and chemotherapeutic response of non-small cell lung cancer patients receiving platinum-containing chemotherapy.ResultsOur investigations found that serum APE1 level was significantly elevated in 229 of 412 NSCLC patients and correlated with its level in tissue (r2 = 0.639, p < 0.001). The elevated APE1 level in both tissue and serum of patients prior to chemotherapy was associated with worse progression-free survival (HR: 2.165, p < 0.001, HR: 1.421, p = 0.012), but not with overall survival. After 6 cycles of chemotherapy, a low APE1 serum level was associated with better overall survival (HR: 0.497, p = 0.010).Experimental DesignWe measured APE1 protein levels in biopsy tissue from 172 NSCLC patients and sera of 412 NSCLC patients receiving platinum-based chemotherapy by immunohistochemistry and a newly established sensitive and specific enzyme-linked immunosorbent assay, respectively. APE1 levels in sera of 523 healthy donors were also determined as control.ConclusionsOur studies indicate that APE1 is a biomarker for predicting prognosis and therapeutic efficacy in NSCLC. The chemotherapy-naïve serum APE1 level, which correlated with its tissue level inversely associated with progression-free survival of platinum-containing doublet chemotherapy, whereas post-treatment serum APE1 level was inversely associated with overall survival.

show abstract

Section: Discussionsupporting

confidence: 63%

Serum APE1 as a predictive marker for platinum-based chemotherapy of non-small cell lung cancer patients

Zhang

Dai

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…In STEMI, inflammatory cells are functionally activated [25, 26]. After PCI, functionally active neutrophil infiltration is aggravated locally in the balloon-injured arteries [27].…”

Section: Discussionmentioning

confidence: 99%

Echocardiographic epicardial fat thickness is a predictor for target vessel revascularization in patients with ST-elevation myocardial infarction

et al. 2016

View full text Add to dashboard Cite

BackgroundThe amount of epicardial adipose tissue (EAT) has been demonstrated to correlate with the severity of coronary artery disease (CAD) and the CAD activity.The aim of this study is to assess the impact of EAT on long term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI).MethodsWe analyzed the data and clinical outcomes of 761 patients (614 males, 57 ± 12 year-old) with STEMI who underwent successful primary PCI from 2003 to 2009. All patients were divided into two groups: thick EAT group, EAT ≥ 3.5 mm and thin EAT group, EAT < 3.5 mm. The primary end points were all-cause death, recurrent MI, target vessel revascularization (TVR) and major cardiac adverse events (MACEs), composite of all-cause death, recurrent MI and TVR, within 5 years.ResultsMedian and mean EAT of 761 patients were 3.3 mm and 3.6 ± 1.7 mm, respectively. Mean follow up period was 46 ± 18 months. MACE-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.001). The event-free survival rate of all-cause death of the thick EAT group was significantly lower than that of the thin EAT group (log-rank P = 0.005). The TVR-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.007). The event-free survival rate of recurrent MI were not significantly different between the groups (log-rank P = 0.206). In the Cox’s proportional hazard model, the adjusted hazard ratio of thick EAT thickness for TVR was 1.868 (95% confidence interval 1.181–2.953, P = 0.008).ConclusionThis study demonstrates that the EAT thickness is related with long term clinical outcome in patients with STEMI. The EAT thickness might provide additional information for future clinical outcome, especially TVR.

show abstract

“…Jin et al found that the levels of APE1/Ref-1 were higher in serum from patients with coronary artery disease than in the serum from control patients. 24 Recently, it has been reported that plasma or urine APE1/Ref-1 levels significantly increase in bladder cancer patients; the area under the curve analysis showed diagnostic values with high specificity and sensitivity. 25 26 Although the underlying mechanisms for secreted APE1/Ref-1 are yet to be fully delineated, a few reports have been able to provide some insight into its biological functions.…”

Section: Extracellularly Secreted Ape1/ref-1 As a Potential Biomarkermentioning

confidence: 97%

Dynamic Regulation of APE1/Ref-1 as a Therapeutic Target Protein

2016

Self Cite

View full text Add to dashboard Cite

Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is a multifunctional protein that plays a central role in the cellular response to DNA damage and redox regulation against oxidative stress. APE1/Ref-1 functions in the DNA base excision repair pathway, the redox regulation of several transcription factors, and the control of intracellular redox status through the inhibition of reactive oxygen species (ROS) production. APE1/Ref-1 is predominantly localized in the nucleus; however, its subcellular localization is dynamically regulated and it may be found in the mitochondria or elsewhere in the cytoplasm. Studies have identified a nuclear localization signal and a mitochondrial target sequence in APE1/Ref-1, as well as the involvement of the nuclear export system, as determinants of APE1/Ref-1 subcellular distribution. Recently, it was shown that APE1/Ref-1 is secreted in response to hyperacetylation at specific lysine residues. Additionally, post-translational modifications such as phosphorylation, S-nitrosation, and ubiquitination appear to play a role in fine-tuning the activities and subcellular localization of APE1/Ref-1. In this review, we will introduce the multifunctional role of APE1/Ref-1 and its potential usefulness as a therapeutic target in cancer and cardiovascular disease.

show abstract

Elevation of the Serum Apurinic/Apyrimidinic Endonuclease 1/Redox Factor-1 in Coronary Artery Disease

Cited by 25 publications

References 23 publications

Serum APE1 as a predictive marker for platinum-based chemotherapy of non-small cell lung cancer patients

Serum APE1 as a predictive marker for platinum-based chemotherapy of non-small cell lung cancer patients

Echocardiographic epicardial fat thickness is a predictor for target vessel revascularization in patients with ST-elevation myocardial infarction

Dynamic Regulation of APE1/Ref-1 as a Therapeutic Target Protein

Contact Info

Product

Resources

About