BackgroundChronic arsenic exposure is associated with cardiovascular abnormalities. Prolongation of the QT (time between initial deflection of QRS complex to the end of T wave) interval and profound repolarization changes on electrocardiogram (ECG) have been reported in patients with acute promyelocytic leukemia treated with arsenic trioxide. This acquired form of long QT syndrome can result in life-threatening arrhythmias.ObjectiveThe objective of this study was to assess the cardiac effects of arsenic by investigating QT interval alterations in a human population chronically exposed to arsenic.MethodsResidents in Ba Men, Inner Mongolia, have been chronically exposed to arsenic via consumption of water from artesian wells. A total of 313 Ba Men residents with the mean arsenic exposure of 15 years were divided into three arsenic exposure groups: low (≤ 21 μg/L), medium (100–300 μg/L), and high (430–690 μg/L). ECGs were obtained on all study subjects. The normal range for QTc (corrected QT) interval is 0.33–0.44 sec, and QTc ≥ 0.45 sec was considered to be prolonged.ResultsThe prevalence rates of QT prolongation and water arsenic concentrations showed a dose-dependent relationship (p = 0.001). The prevalence rates of QTc prolongation were 3.9, 11.1, 20.6% for low, medium, and high arsenic exposure, respectively. QTc prolongation was also associated with sex (p < 0.0001) but not age (p = 0.486) or smoking (p = 0.1018). Females were more susceptible to QT prolongation than males.ConclusionsWe found significant association between chronic arsenic exposure and QT interval prolongation in a human population. QT interval may potentially be useful in the detection of early cardiac arsenic toxicity.

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miR-154 has been proven to act as a tumor suppressor in several types of tumors. However, its role in non-small cell lung cancer (NSCLC) remains unclear. Thus, the aim of this study was to investigate the effects of miR-154 on NSCLC tumorigenesis and development. Using real-time quantitative PCR (qRT-PCR), we analyzed expression of miR-154 at the transcriptional level in 40 NSCLC tumor tissues and matched adjacent normal tissues and the correlation with clinicopathological features of the patients. The miR-154 mimic was stably transfected into NSCLC A549 cells, and the effects of miR-154 on cancer cell proliferation, colony formation, cell cycle arrest, apoptosis, migration and invasion in vitro, and on the growth of in vivo xenografts were investigated. miR-154 expression levels were significantly downregulated in the NSCLC compared to the corresponding non-cancerous lung tissues (P<0.05), and decreased miR-154 expression was significantly associated with metastasis (P<0.001), larger tumor size (P<0.001) and advanced TNM stage (P<0.001). Furthermore, transfection of the miR-154 mimic into the NSCLC A549 cells was able to inhibit cell proliferation, colony formation, invasion and migration, and induce cell apoptosis and G0/G1 cell cycle arrest. Enforced expression of miR-154 also suppressed the growth of cancer cell xenografts in vivo. These findings indicate that miR-154 may become a potential target for miR-based therapy of NSCLC.

Background: The HOXA cluster antisense RNA 2 (HOXA-AS2) has recently been discovered to be involved in carcinogenesis in multiple cancers. However, the role and underlying mechanism of HOXA-AS2 in non-small cell lung cancer (NSCLC) yet need to be unraveled. Methods: HOXA-AS2 expression in NSCLC tissues and cell lines was detected using quantitative real-time PCR (qRT-PCR). Furthermore, the effects of HOXA-AS2 on NSCLC cell proliferation, apoptosis, migration, and invasion were assessed by MTS, flow cytometry, wound healing and transwell invasion assays, respectively. Starbase2.0 predicted and luciferase reporter and RNA immunoprecipitation (RIP) assays were used to validate the association of HOXA-AS2 and miR-520a-3p in NSCLC cells. Results: Our results revealed that HOXA-AS2 in NSCLC tissues were up-regulated and cell lines, and were associated with poor prognosis and overall survival. Further functional assays demonstrated that HOXA-AS2 knockdown significantly inhibited NSCLC cell proliferation, induced cell apoptosis and suppressed migration and invasion. Starbase2.0 predicted that HOXA-AS2 sponge miR-520a-3p at 3′-UTR, which was confirmed using luciferase reporter and RIP assays. miR-520a-3p expression was inversely correlated with HOXA-AS2 expression in NSCLC tissues. In addition, miR-520a-3p inhibitor attenuated the inhibitory effect of HOXD-AS2-depletion on cell proliferation, migration and invasion of NSCLC cells. Moreover, HOXA-AS2 could regulate HOXD8 and MAP3K2 expression, two known targets of miR-520a-3p in NSCLC. Conclusion: These findings implied that HOXA-AS2 promoted NSCLC progression by regulating miR-520a-3p, suggesting that HOXA-AS2 could serve as a therapeutic target for NSCLC.

Breast cancer (BC) is the most common malignancy in women. Due to BC heterogeneity, complexity, and metastasis, many BC patients do not successfully respond to therapies. The effective management of BC depends on early diagnosis and monitoring of drug response. Therefore, identifying new biomarkers for the diagnosis, prognosis, and development of new drugs is urgently required. Dysregulation of microRNAs (miRNAs) participates in the tumorigenesis and progression of cancers, especially breast cancer (BC). Several studies demonstrated that miRNAs could perform their function as oncogenes or tumor suppressors. This review describes recent progress on the role of microRNAs in the diagnosis, prognosis, hallmark, and treatment of BC. According to a recent literature survey, miRNAs play a pivotal role in the regulation of hallmarks of cancer, such as proliferation, apoptosis, invasion, metastasis, and tumor stemness. Many miRNAs are potential biomarkers for BC for diagnosis, and some are indicators of prognosis. Moreover, circulating miRNA profiles, as minimally invasive, diagnostic, and prognostic markers, are broadly used in BC therapy, and some miRNAs are good predictors of therapeutic outcomes. Other miRNAs are involved in overcoming chemoresistance and in increasing BC drug sensitivity.

This study suggests that IMRT results in milder hematological toxicity than either 3DCRT or RapidARC. Dosimetric parameters were associated with the incidence of HT in cervical cancer patients who received concurrent chemoradiotherapies.