MicroRNAs (miRNAs) are small, non-coding RNAs found throughout the eukaryotes that control the expression of a number of genes involved in commitment and differentiation of hematopoietic stem cells and tumorigenesis. Widespread dysregulation of miRNAs have been found in hematological malignancies, including human acute myeloid leukemia (AML). A comprehensive understanding of the role of miRNAs within the complex regulatory networks that are disrupted in malignant AML cells is a prerequisite for the development of therapeutic strategies employing miRNA modulators. Herein, we review the roles of emerging miRNAs and the miRNAs regulatory networks in AML pathogenesis, prognosis, and miRNA-directed therapies.

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Our data showed that TRAF1 was significantly upregulated in NSCLC tissues. TRAF1 expression was positively associated with NSCLC lymphatic metastasis and clinical stage and was negatively associated with overall patient survival. TRAF1 promoted NSCLC cell proliferation CONCLUSION: TRAF1 expression was positively associated with NSCLC lymphatic metastasis and histological grade and was negatively associated with overall patient survival. TRAF1 may be an important therapeutic target for NSCLC.

Long non-coding RNAs (lncRNAs) have important roles in the development and progression of various types of human cancer. However, the expression and function of the lncRNA prostate cancer-associated non-coding RNA 1 (PRNCR1) in breast cancer remains unclear. Reverse transcription-quantitative PCR was performed to measure the levels of mRNA expression. Cell counting kit-8, flow cytometry, wound healing and Transwell assays were also performed to study cell proliferation, cell cycle, migration and invasion, respectively. The results of the present study revealed that PRNCR1 expression levels were higher in breast cancer tissues compared with adjacent normal tissues in a patient study. It was also determined that high expression of PRNCR1 was significantly associated with advanced clinical stage, positive metastasis and poor prognosis for patients with breast cancer. In vitro experiments determined that PRNCR1 was significantly upregulated in the breast cancer cell lines BT-549, MCF-7, SK-BR-3 and MDA-MB-231 compared with the normal human breast cell line, MCF-10A. Silencing of PRNCR1 significantly inhibited the proliferation, colony formation, cell cycle progression, migration and invasion of SK-BR-3 and BT-549 cells, while cell apoptosis was induced. In addition, knockdown of PRNCR1 suppressed epithelial-mesenchymal transition in SK-BR-3 and BT-549 cells. In summary, the present results demonstrated that lncRNA PRNCR1 was significantly upregulated in breast cancer and was associated with cancer progression and poor patient prognosis. In vitro experiments determined that knockdown of PRNCR1 inhibited the malignant phenotypes of breast cancer cells. Taken together, the results indicated that PRNCR1 may be used as a potential therapeutic target for patients with breast cancer.

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