ABSTRACT
An increasing number of people die from breast cancer every year. Consequently, more research has been concentrated on the study of this type of tumour, and miR-373 resulted as an important gene for treating breast cancer. To explore the influence of miR-373 on the invasion and migration of breast cancer and the expression level of target gene TXNIP, a set of therapeutic methods were designed based on miR-373. The transfection was performed using miR-373 inhibitor; the concentration of miR-373 was controlled by inhibitor, and it was transfected into MCF-7 cell by lipofectin. Fluorescent quantitative polymerase chain reaction was used to detect the expression level of miR-373 in cells after transfection as well as that of Caspase-3 and Caspase-8. MTT assay was used to detect the influence of miR-373 inhibitor on MCF-7 cells. The expression quantity of miR-373 in cell and tissue of breast cancer with high-low invasion and migration ability was detected by qRT-PCR (quantitative real-time polymerase chain reaction), thus the influence of the expression quantity of miR-373 on the invasion and migration of cell was determined. The expression of miR-373, EMT and TXNIP was determined by Western blot. Through the identification of proteomics and bioinformatics, it was finally found that TXNIP was regulated by miR-373. The protein expression level of TXNIP was negatively correlated with the level of miR-373. Thus it was concluded that miR-373 could promote the invasion and migration of breast cancer. In addition, in the tissue and cell of breast cancer with different invasion and migration abilities, the expression level of TXNIP was negatively correlated with the level of miR-373.
Subject(s)
Breast Neoplasms/pathology , Carrier Proteins/physiology , Gene Expression Regulation, Neoplastic , MicroRNAs/physiology , Neoplasm Proteins/physiology , RNA, Neoplasm/physiology , Adenocarcinoma/pathology , Breast Neoplasms/genetics , Breast Neoplasms/metabolism , Carrier Proteins/biosynthesis , Carrier Proteins/genetics , Caspase 3/biosynthesis , Caspase 3/genetics , Caspase 9/biosynthesis , Caspase 9/genetics , Cell Line, Tumor , Female , Humans , MicroRNAs/antagonists & inhibitors , Neoplasm Proteins/biosynthesis , Neoplasm Proteins/genetics , RNA, Messenger/biosynthesis , RNA, Neoplasm/antagonists & inhibitors , RNA, Neoplasm/biosynthesis , Transfection , Up-RegulationABSTRACT
Different pharmaceutical preparations against the common cold contain acetaminophen, phenylephrine hydrochloride, and chlorpheniramine maleate. A degradation product had been discovered in these preparations after short- and long-term stability studies. This degradation product was isolated and found to be an adduct of phenylephrine and maleic acid. An account of the isolation and characterization of this compound was published. Our interest in this area led us to synthesize the compound, and we found that the synthesized compound does not have the same spectroscopic properties described in the original paper. Our subsequent work identified the structure of the degradation product as a "Michael addition" product of phenylephrine and maleic acid.
