Traditionally, destruction of DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] for environmental remediation required high-energy processes such as incineration. Here, the capability of powdered zero-valent iron to dechlorinate DDT and related compounds at room temperature was investigated. Specifically, DDT, DDD [1,1-dichloro-2,2-bis(p-chlorophenyl)ethane], and DDE [2,2-bis(p-chlorophenyl)-1,1-dichloroethylene] transformation by powdered zero-valent iron in buffered anaerobic aqueous solution was studied at 20 °C, with and without the presence of nonionic surfactant Triton X-114. The iron was successful at dechlorinating DDT, DDD, and DDE. The rates of dechlorination of DDT and DDE were independent of the amount of iron, with or without surfactant. The rates with surfactant present were much higher than without. Initial first-order transformation rates for DDT, DDD, and DDE were determined. For example, the initial first-order rate of DDT dechlorination was 1.7 ± 0.4 and 3.0 ± 0.8 day-1 or, normalized by the specific iron surface area, 0.016 ± 0.004 and 0.029 ± 0.008 L m-2 h-1, without and with surfactant, respectively. A mechanistic model was constructed that qualitatively fit the observed kinetic data, indicating that the rate of dechlorination of the solid-phase (crystalline) reactants was limited by the rate of dissolution into the aqueous phase.

MicroRNAs (miRNAs) are a group of small non-coding RNAs that modulate post-transcriptional gene expression. It has been demonstrated that various miRNAs may be expressed at different levels in different types of tumors. The present study assessed the role of microRNA-148a-3p (miR-148a-3p) in epithelial ovarian cancer (EOC). The results demonstrated that miR-148a-3p was decreased in EOC tissues and that a lower miRa-148-3p concentration was associated with a higher overall survival rate. Transfection of miR-148a-3p suppressed the invasive and proliferative capacity of SKOV3 cells. The induced overexpression of miR-148a-3p significantly inhibited the relative luciferase activity of the pmirGLO-c-Met-3′untranslated region compared with an empty vector. In addition, c-Met silencing led to a decrease in the invasive and proliferative capacity of EOC cells. The inhibition of miR-148a-3p did not increase the invasiveness of SKOV3 cells, even when c-Met was silenced. To the best of our knowledge, the present study is the first to demonstrate that miR-148a-3p expression is decreased in EOC cancer tissues and cell lines. The present study therefore demonstrated that miR-148a-3p may serve as a tumor suppressor in EOC by targeting c-Met.

The abnormal expression of microRNAs (miRNAs/miRs) has been widely reported in various tumor types. miR-217 was demonstrated to be aberrantly expressed in a number of tumors, including pancreatic adenocarcinoma and osteosarcoma; however, its specific expression pattern has never been investigated in cervical cancer cells. Compared with normal control, the level of Rho-associated protein kinase 1 (ROCK1) expression was markedly increased in cervical cancer tissues and cells compared with that in non-cancerous tissues and cells. The expression of miR-217 was significantly reduced in cervical cancer tissues and cell lines. Overexpression of miR-217 could suppress colony formation and the cell invasion capacity of SiHa and HeLa cells. Flow cytometry indicated that miR-217 significantly increased cell apoptosis in SiHa and HeLa cells. Dual-luciferase reporter assays demonstrated that ROCK1 was a target gene of miR-217. In addition, overexpression of ROCK1 also led to an increased invasion capacity in SiHa cells, even when miR-217 was inhibited, indicating that the anti-invasive effects of miR-217 were mediated through ROCK1. In summary, the results of the present study indicated that miR-217 functions as a tumor suppressor in cervical cancer cells, primarily by targeting ROCK1.