Purpose This study aimed to investigate the changes in microRNA-130a (miR-130a) and its correlation with cardiotoxicity during epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D+T) adjuvant chemotherapy in human epidermal growth factor receptor-2-positive (HER2 + ) breast cancer patients. Methods A total of 72 HER2 + breast cancer patients who underwent resection and were scheduled to receive EC-D+T adjuvant therapy were consecutively enrolled. The expression of miR-130a and cardiotoxicity (defined as any of the following situations: 1) absolute decline of left ventricular ejection fraction (LVEF) ≥ 10% and LVEF < 53%; 2) heart failure; 3) acute coronary artery syndromes; and 4) fatal arrhythmia) were assessed every 3 months throughout the 15-month EC-D+T treatment. Results The accumulating cardiotoxicity rate was 12 (16.7%), of which the incidence of heart failure, acute coronary syndrome, life-threatening arrhythmias, ΔLVEF ≥ 10%, and LVEF < 53% was 0 (0.0%), 1 (1.4%), 0 (0.0%), and 12 (16.7%), respectively. Baseline miR-130a expression was negatively correlated with LVEF (%) and positively correlated with cardiac troponin I. The expression of miR-130a gradually increased in both cardiotoxicity and non-cardiotoxicity patients during EC-D+T treatment, while the increment of miR-130a was more obvious in cardiotoxicity patients compared with non-cardiotoxicity patients. Further logistic regression and receiver operating characteristic curve analysis indicated that miR-130a was an independent predictive factor for increased cardiotoxicity risk. Conclusion MiR-130a increases constantly and predicts high cardiotoxicity risk during EC-D+T adjuvant chemotherapy in HER2 + breast cancer patients.

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Background MicroRNA‐34a (miR‐34a) plays an essential role in regulating blood lipid, inflammation, cell adhesion molecules, and atherosclerosis, the latter factors are closely involved in the etiology of coronary heart disease (CHD). However, the clinical value of miR‐34a in CHD patients' management is rarely reported. Hence, this study aimed to assess the correlation of miR‐34a with disease risk, blood lipid, coronary artery stenosis, inflammatory cytokines, and cell adhesion molecules of CHD. Methods A total of 203 CHD patients and 100 controls were recruited in this study, then their plasma samples were collected to detect the miR‐34a by reverse transcription quantitative polymerase chain reaction. Furthermore, serum samples from CHD patients were obtained for inflammatory cytokines and cell adhesion molecule measurement by enzyme‐linked immunosorbent assay. Results MiR‐34a was elevated in CHD patients compared to controls (p < 0.001) and it disclosed a good diagnostic value of CHD (area under curve: 0.899, 95% confidence interval: 0.865–0.934). Besides, miR‐34a positively correlated with triglyceride (p < 0.001), total cholesterol (p = 0.022) and low‐density lipoprotein cholesterol (p = 0.004), but not with high‐density lipoprotein cholesterol (p = 0.110) in CHD patients. Moreover, miR‐34a associated with Gensini score in CHD patients (p < 0.001). As to inflammation‐related indexes and cell adhesion molecules, MiR‐34a expression was positively linked with C‐reactive protein (p < 0.001), tumor necrosis factor alpha (p = 0.005), interleukin (IL)‐1β (p = 0.020), IL‐17A (p < 0.001), vascular cell adhesion molecule‐1 (p < 0.001), and intercellular adhesion molecule‐1 (p = 0.010) in CHD patients, but not with IL‐6 (p = 0.118) and IL‐10 (p = 0.054). Conclusion MiR‐34a might serve as a biomarker in assistance of diagnosis and management of CHD.

Objective Long non‐coding RNA KQT‐like subfamily, member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) could regulate lipid metabolism, vascular smooth muscle cell function, inflammation, and atherosclerosis. This study aimed to evaluate whether lncRNA KCNQ1OT1 could serve as a biomarker for reflecting coronary heart disease (CHD) patients' disease situation and prognosis. Methods LncRNA KCNQ1OT1 expression was determined in peripheral blood mononuclear cells from 267 CHD patients, 50 disease controls (DCs) (unexplained chest pain), and 50 healthy controls (HCs) by the RT‐qPCR method. TNF‐α, IL‐17A, VCAM‐1, and ICAM‐1 were determined by the ELISA procedure in serum from CHD patients only. The mean (95% confidential interval) follow‐up duration was 16.0 (15.3–16.8) months. Results LncRNA KCNQ1OT1 was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). LncRNA KCNQ1OT1 could distinguish the CHD patients from DCs (area under the curve [AUC]: 0.757) and from the HCs (AUC: 0.880). LncRNA KCNQ1OT1 was positively associated with triglyceride (p = 0.026), low‐density lipoprotein cholesterol (p = 0.023), cardiac troponin I (p = 0.023), and C‐reactive protein (p = 0.001). Besides, lncRNA KCNQ1OT1 was also positively linked with the Gensini score (p = 0.008). Furthermore, lncRNA KCNQ1OT1 was positively related to the TNF‐α (p < 0.001), IL‐17A (p = 0.008), and VCAM‐1 (p = 0.003). LncRNA KCNQ1OT1 was elevated in CHD patients with MACE compared to those without MACE (p = 0.006); moreover, lncRNA KCNQ1OT1 high was associated with shorter MACE‐free survival (p = 0.018). Conclusion Circulating lncRNA KCNQ1OT1 expression not only reflects the stenosis degree, blood lipid level, and inflammation status but also predicts the MACE risk, while a large‐scale study is needed for verification.