Additionally, fluoxetine could inhibit the phosphatidylinositol 3‑kinase‑protein kinase B (PI3K‑AKT) signaling pathway, whereas LY294002, a specific inhibitor of PI3K, suppressed the function of PI3K‑AKT signaling and suppressed the expression levels of glucose metabolism‑associated proteins, including GSK‑3β, G6PC, PEPCK and FOXO1 in BRL‑3A cells. The results of the present study revealed that fluoxetine may regulate glucose and lipid metabolism via the PI3K‑AKT signaling pathway in diabetic rats.Menin‑mixed‑lineage leukemia (MLL) inhibitors have potential for use as therapeutic agents for MLL‑rearranged leukemia. They are also effective against solid cancers, such as breast cancer. The present study demonstrated that menin‑MLL inhibitors, such as MI‑463, unexpectedly induced the ferroptotic cell death of several cancer cell lines. MI‑463 at a double‑digit nM concentration markedly decreased the viable number of OVCAR‑8 ovarian cancer cells for 3 days. Ferrostatin‑1 (a ferroptosis inhibitor) almost completely abrogated the MI‑463‑induced decrease in viable cell numbers. check details Furthermore, the cancer cell‑killing activity was inhibited by N‑acetylcysteine [a scavenger of reactive oxygen species (ROS)], deferoxamine (DFO, an iron chelator), PD146176 (a specific inhibitor of arachidonate 15‑lipoxygenase), idebenone (a membrane‑permeable analog of CoQ10) and oleic acid [a monounsaturated fatty acid and one of the end products of stearoyl‑CoA desaturase 1 (SCD1)], whereas Z‑VAD‑FMK (an apoptosis inhibitor) had apresent an effective therapeutic approach for several types of cancer via the induction of ferroptosis.Progranulin (PGRN) is a secreted growth factor involved in pleiotropic functions, particularly angiogenesis. A distinctly different placental expression of PGRN has been reported between normal pregnancies and pregnancies with complications, such as pre‑eclampsia or fetal growth restriction. However, the role of PGRN in placental vascular development remains to be elucidated. In the present study, PGRN‑knockout mice (PGRN‑/‑) were used to investigate the role of PGRN in the development of placental blood vessels and placental formation. Placental weights and pup body weights were significantly lower in the PGRN‑/‑ mice compared with the wild‑type mice. Reduced labyrinthine layer areas and aberrant vascularization were also observed via hematoxylin and eosin staining of PGRN‑/‑ mice at embryonic day 14.5 (E14.5) and E17.5. In addition, the morphological data obtained via immunohistochemistry, immunofluorescence staining and western blotting demonstrated decreased expression levels of the blood vessel markers α‑smooth muscle actin and CD31 in PGRN‑/‑ placentas. Furthermore, vasodilator endothelial nitric oxide synthase was reduced in the PGRN‑/‑ placenta. These results indicated that PGRN serves an essential role in the normal angiogenesis of the placental labyrinth in mice.In recent years, there have been major breakthroughs in immunotherapies for the treatment of cancer. However, different patients have different responses to immunotherapy. Numerous studies have shown that the accumulation of epigenetic abnormalities, such as DNA methylation, serve an important role in the immune response of lung adenocarcinoma (LUAD). To investigate the effects of DNA methylation on tumor immunity with survival and prognosis, relevant studies can be performed based on the regulatory mechanisms of RNA molecules. For example, long non‑coding RNAs (lncRNAs), which regulate gene expression through epigenetic levels. By constructing an immune-associated competitive endogenous RNA (ceRNA) network, the present study identified the regulatory associations among 3 key immune‑associations mRNAs, 2 microRNAs (miRs) and 29 lncRNAs that were closely associated with the prognosis of patients with LUAD. The molecular biology analysis indicated that hypomethylation of the 1101320‑1104290 regions of chromosome 1 resulted in the low expression levels of LINC00337 and that LINC00337 may affect the expression levels of CHEK1 by competitively binding with human (has)‑miR‑373 and hsa‑miR‑195. Therefore, abnormal DNA methylation in lncRNA‑associated regions caused their abnormal expression levels, which further affected the interactions between RNA molecules. The interactions between these RNA molecules may have regulatory effects on tumor immunity and the prognosis of patients with LUAD.Multidrug resistance (MDR) is a major cause of disease relapse and mortality in breast cancer. Paired‑related homeobox 1 (PRRX1) is associated with the epithelial‑mesenchymal transition (EMT), which is involved in tumor development, including cell invasion and MDR. However, the effect of PRRX1 on MDR had not clearly established. The present study investigated the influence of PRRX1 on MDR and the underlying molecular mechanisms in MCF‑7 breast cancer cells. MCF‑7 cells were divided into PRRX1+ group (cells transfected with a recombinant plasmid carrying the PRRX1 gene), negative control group (cells transfected with a blank vector) and blank group (untreated cells). It was found that the relative protein and mRNA expression levels of PRRX1, N‑cadherin, vimentin and P‑glycoprotein were significantly higher in PRRX1‑overexpressing MCF‑7 cells compared with those in control cells. The half‑maximal inhibitory concentration of three groups after treatment with docetaxel and cis‑platinum complexes were significantly higher in PRRX1‑overexpressing MCF‑7 cells compared with those in control cells. Furthermore, relative PTEN expression decreased significantly and levels of phosphorylated PI3K and AKT increased substantially in PRRX1‑overexpressing MCF‑7 cells. These results indicated that PRRX1 overexpression may induce MDR via PTEN/PI3K/AKT signaling in breast cancer. It is highly recommended that PRRX1 gene expression detection should be performed in patients with breast cancer to aid the selection of more appropriate treatments, which will lead to an improved prognosis in clinical practice.