Evaluation of miR-9 and miR-143 expression in urine specimens of sulfur mustard exposed patients

Khafaei, Mostafa; Samie, Shahram; Mowla, Seyed Javad; Alvanegh, Akbar Ghorbani; Mirzaei, Behnaz; Chavoshei, Somaye; Dorraj, Ghamar Soltan; Esmailnejad, Mostafa; Tavallaie, Mahmood; Nourani, Mohammadreza

doi:10.1515/intox-2015-0026

Cited by 8 publications

(10 citation statements)

References 32 publications

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“…miRNAs, the important genetic regulatory factors in humans, have been reported to exert regulatory effects on the occurrence and development of liver carcinoma ( 13 ). Nevertheless, the mechanism of miR-143 involved in the development of liver carcinoma remains to be determined ( 14 ). Thus, in this study, we preliminarily investigated the mechanism how miR-143 affects the development of liver carcinoma.…”

Section: Discussionmentioning

confidence: 99%

The mechanism of miR-143 inducing apoptosis of liver carcinoma cells through regulation of the NF-κB pathway

Zheng

Yang

et al. 2018

Oncol Lett

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Primary hepatic carcinoma is a common malignant tumor with poor treatment efficacy. The effect and mechanism of miR-143 in apoptosis of liver carcinoma cells were investigated in the present study. In vitro transfection of liver carcinoma SMMC-7721 cells was performed using artificially synthesized miR-143 mimics. The proliferation of liver carcinoma cells that were treated was detected by MTT assay. Liver carcinoma cells were then stained using the Annexin V-FITC/PI method, and the apoptosis of stained liver carcinoma cells was measured using a flow cytometer. The relative mRNA expression of NF-κB p65 in the intervention and control groups was assayed using reverse transcription-quantitative polymerase chain reaction, and the protein expression of NF-κB p65 was detected using western blot analysis. The results showed that, in the intervention group, the proliferation rate of cells transfected using miR-143 mimics was significantly lower than that in the control group, the number of apoptotic SMMC-7721 cells in the intervention group increased, and the protein expression of NF-κB p65 was decreased. Thus, miR-143 may downregulate the protein expression of NF-κB p65, thereby triggering the NF-κB signaling transduction pathway inducing apoptosis of liver carcinoma cells.

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Section: Discussionmentioning

confidence: 99%

The mechanism of miR-143 inducing apoptosis of liver carcinoma cells through regulation of the NF-κB pathway

Zheng

Yang

et al. 2018

Oncol Lett

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“…miRNA higher expression result in abnormal proliferation and migration of tumor cells ( 12 ). Extensive studies on miRNAs revealed that the expression levels of miR-143 in many tumor cells were significantly lower than normal tissues ( 13 , 14 ).…”

Section: Discussionmentioning

confidence: 99%

Study of miR-143 expression in stomach cancer

Huang

Zhu

et al. 2018

Oncol Lett

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The present study was planned to investigate miR-143 expression during stomach cancer. The study explored the relationship between miR-143 expression and clinicopathological characteristics including proliferation, migration and apoptosis of stomach cancer cells. Sixty-three samples from each of stomach cancer tissue and surrounding tissue were obtained. Total RNA was extracted. The expression levels of miR-143 from stomach cancer tissue as well as from surrounding tissue were measured by semi-quantitative PCR. The effects of miR-143 overexpression on the migration of stomach cancer cells were examined by Transwell assay. The effects of miR-143 overexpression on the apoptosis of stomach cancer cells were examined by flow cytometer. The expression level of miR-143 was significantly decreased in stomach cancer tissues in comparison to surrounding tissues (P<0.01). Moreover, the expression of miR-143 related well with the tumor size, TNM stage, lymphatic metastasis and relapse (P<0.01). On the other hand, stomach cancer cell line with overexpression of miR-143, showed significant decline in proliferation rate and migration rate comparison to control cells (P<0.01). However, it showed significant higher in apoptosis rate (P<0.01). The present study concluded that expression of miR-143 is low during stomach cancer. Further, higher expression levels of miR-143 have the ability to decline proliferation and migration of stomach cancer cells. In this manner, the expression level of miR-143 could be used as an important factor to determine the severity of stomach cancer.

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“…Analogously, it has been reported in the sulfur mustard-resistant HaCaT human keratinocyte line (109) that changes of miRNA profile are pivotal for sulfur mustard-resistance (110) and that some of them are also critical for resistance to alkylating agent cisplatin (111). Another study addressing miRNA-9 and miRNA-143 in the urine of 32 sulfur mustard-injured patients and 32 healthy individuals reported their significant reduced excretion correlated with the ongoing post-exposure pathogenicity (112). These two miRNAs have been assigned to the regulation of central signalling pathways (MAPK, TGF-, Wnt, etc) and their down-regulation specifically associated with the reduction of the inflammation suppressing factor TGF-, thus conferring mechanistic support to the inflammatory response of mustard-induced pathology.…”

Section: Epigenetics In the Management Of Long-term Toxicity Of Vesicmentioning

confidence: 72%

Impact of melatonin effects on toxicology of vesicant chemical warfare agents: When science meets reality

Romero¹,

Gil‐Martín²,

Rı́os³

et al. 2020

Melatonin Res.

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In this review we focused our attention on sulfur mustard [bis(2-chloroethyl) sulphide], the main vesicant chemical warfare agent (CWA), which has been widely used in different military conflicts, including World War I and the Iran-Iraq war. Moreover, the evolution of the recent Iraq and Syria conflicts suggests that terrorist groups are aware of the significant psychological and media effects that would be produced by the mere attempt to use CWAs. Sulfur mustard can produce the alkylation of macromolecules bearing sulfhydryl groups, such as DNA and proteins. This vesicant can also generate free radicals which can develop toxicity in the areas exposed, such as the eyes, skin, respiratory tract (inhalation) and gastrointestinal tract (ingestion). In this respect, we advance and propose three salvage mechanisms through which a broad-spectrum multipotent molecule, melatonin, could facilitate neutralization of the toxic damage induced by sulfur mustard radical scavenging. We also speculate that the long-term effects of varying severity can appear after acute poisoning. Besides, melatonin-based therapy strategies can modulate of epigenetic mechanisms and become very suitable for the clinical treatment of victimized patients. However, the utilization of melatonin as a “therapeutic bullet” addressed to counteract the vesicant CWAs needs much additional in vitro research as well as systematic animal studies and controlled translational trials.

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Evaluation of miR-9 and miR-143 expression in urine specimens of sulfur mustard exposed patients

Cited by 8 publications

References 32 publications

The mechanism of miR-143 inducing apoptosis of liver carcinoma cells through regulation of the NF-κB pathway

The mechanism of miR-143 inducing apoptosis of liver carcinoma cells through regulation of the NF-κB pathway

Study of miR-143 expression in stomach cancer

Impact of melatonin effects on toxicology of vesicant chemical warfare agents: When science meets reality

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