摘要
Background Gigantomastia is the overdevelopment of the female mammary gland, and it causes great physiological and psychological burdens to patients. A better understanding of the molecular mechanisms involved in gigantomastia is needed to develop less invasive and more effective medical treatments. MicroRNA （miRNA） is a class of small noncoding RNAs that play an important regulatory role at the post-transcriptional level. These miRNAs are known to be involved in many diseases, including breast cancer; however, the relationship between miRNA and gigantomastia is largely unknown. Methods Whole genome-wide expression of miRNA and mRNA in gigantomastia was detected using microarray and functional annotation was performed based on the altered expression of miRNAs and mRNAs. Results We found many miRNAs and mRNAs to be significantly differentially expressed in gigantomastia compared with normal breast tissues. Functional annotation analysis indicated that APK, Wnt, and Neurotrophin signaling pathways may participate in gigantomastia. Conclusion This study addresses the need for better diagnosis and treatment of gigantomastia by providing new insight into the molecular mechanisms underlying this disease.
Background Gigantomastia is the overdevelopment of the female mammary gland, and it causes great physiological and psychological burdens to patients. A better understanding of the molecular mechanisms involved in gigantomastia is needed to develop less invasive and more effective medical treatments. MicroRNA （miRNA） is a class of small noncoding RNAs that play an important regulatory role at the post-transcriptional level. These miRNAs are known to be involved in many diseases, including breast cancer; however, the relationship between miRNA and gigantomastia is largely unknown. Methods Whole genome-wide expression of miRNA and mRNA in gigantomastia was detected using microarray and functional annotation was performed based on the altered expression of miRNAs and mRNAs. Results We found many miRNAs and mRNAs to be significantly differentially expressed in gigantomastia compared with normal breast tissues. Functional annotation analysis indicated that APK, Wnt, and Neurotrophin signaling pathways may participate in gigantomastia. Conclusion This study addresses the need for better diagnosis and treatment of gigantomastia by providing new insight into the molecular mechanisms underlying this disease.
