Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG‑AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG‑AS1 in breast cancer. To achieve this, the expression of MAFG‑AS1, microRNA (miR)‑150‑5p and MYB was detected by reverse transcription‑quantitative PCR. The binding between miR‑150‑5p and MAFG‑AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG‑AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG‑AS1 expression promoted the proliferation, migration and epithelial‑mesenchymal transition of breast cancer cells. By contrast, miR‑150‑5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR‑150‑5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG‑AS1 served as a sponge of miR‑150‑5p, and that miR‑150‑5p bound to MYB. The functional rescue assay results demonstrated that MAFG‑AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR‑150‑5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG‑AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR‑150‑5p/MYB axis, which suggested that MAFG‑AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.The cyclin D binding myb‑like transcription factor 1 (DMTF1), a haplo‑insufficient tumor suppressor gene, has 3 alternatively spliced mRNA isoforms encoding DMTF1α, β and γ proteins. Previous studies have indicated a tumor suppressive role of DMTF1α and the oncogenic activity of DMTF1β, while the function of DMTF1γ remains largely undetermined. In the present study, the mechanisms regulating DMTF1 isoform expression were investigated and the functional interplay of DMTF1β and γ with DMTF1α was characterized.  https://www.selleckchem.com/products/Docetaxel(Taxotere).html  It was found that specific regions of DMTF1β and γ transcripts can impair their mRNA integrity or stability, and thus reduce protein expression levels. Additionally, DMTF1β and γ proteins exhibited a reduced stability compared to DMTF1α and all 3 DMTF1 isoforms were localized in the nuclei. Two basic residues, K52 and R53, in the DMTF1 isoforms determined their nuclear localization. Importantly, both DMTF1β and γ could associate with DMTF1α and antagonize its transactivation of the ARF promoter. Consistently, the ratios of both DMTF1β/α and γ/α were significantly associated with a poor prognoses of breast cancer patients, suggesting oncogenic roles of DMTF1β and γ isoforms in breast cancer development.Serpin family E member 1 (SERPINE1), a serine proteinase inhibitor, serves as an important regulator of extracellular matrix remodeling. Emerging evidence suggests that SERPINE1 has diverse roles in cancer and is associated with poor prognosis. However, the mechanism via which SERPINE1 is induced in cancer has not been fully determined. In order to examine the molecular mechanism of SERPINE1 expression, the present study took advantage of the isogenic pair of lung cancer cells with epithelial or mesenchymal features. Using genetic perturbation and following biochemical analysis, the present study demonstrated that SERPINE1 expression was upregulated in mesenchymal lung cancer cells and promoted cellular invasiveness. Yes‑associated protein (YAP)‑dependent SERPINE1 expression was modulated by treatment with a Rho‑associated protein kinase inhibitor, Y27632. Moreover, TGFβ treatment supported YAP‑dependent SERPINE1 expression, and an enhanced TGFβ response in mesenchymal lung cancer cells promoted SERPINE1 expression. TGFβ‑mediated SERPINE1 expression was significantly attenuated by knockdown of YAP or transcriptional co‑activator with PDZ‑binding motif, suggesting that crosstalk between the TGFβ and YAP pathways underlies SERPINE1 expression in mesenchymal cancer cells.Mammalian target of rapamycin (mTOR) serves an important role in regulating various biological processes, including cell proliferation, metabolism, apoptosis and autophagy. Among these processes, energy metabolism is the dominant process. The metabolism of not only amino acids, fatty acids and lipids, but also that of nucleotides and glucose has been indicated to be regulated by mTOR. Aerobic glycolysis, which is a specific form of glucose metabolism, is prevalent in carcinomas, and it has been considered to be a potential target for cancer therapy. In reviewing the complexity of the mTOR pathway, it is important to elucidate the central role and detailed pathway via which mTOR regulates glycolysis. In the present study, the complex mechanisms via which mTOR regulates aerobic glycolysis were comprehensively reviewed to highlight the potential of drug development via targeting the molecules associated with mTOR and glycolysis and to further provide strategies for the clinical treatment of cancer.W922, a novel PI3K/Akt/mTOR pathway inhibitor, exhibits efficient anti‑tumor effects on HCT116, MCF‑7 and A549 human cancer cells compared with other synthesized compounds. The present study aimed to investigate its anti‑tumor effects on colorectal cancer cells. A total, of seven different colorectal cell lines were selected to test the anti‑proliferation profile of W922, and HCT116 was found to be the most sensitive cell line to the drug treatment. W922 inhibited HCT116 cell viability and cell proliferation in vitro in concentration‑ and time‑dependent manners. Furthermore, W922 suppressed the tumor growth in a xenograft mouse model and exhibited low toxicity. The proteomic alterations in W922‑treated HCT116 cells were found to be associated with cell cycle arrest, negative regulation of signal transduction and lysosome‑related processes. W922 caused cell cycle arrest of HCT116 cells in G0‑G1 phase, but only triggered slight apoptosis. In addition, the PI3K/Akt/mTOR signaling proteins were dephosphorylated upon W922 treatment.