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The protein and mRNA levels of spliced XBP1 were also increased, and the level of MUC5AC protein was notably increased. The ROS scavenger NAC and ER stress inhibitor 4‑PBA were found to reduce ER stress‑associated protein expression and MUC5AC production and secretion. Further analyses revealed that MUC5AC secretion was also attenuated by IRE1α and XBP1 siRNAs, accompanied by a decreased mRNA expression of spliced XBP1. Taken together, these results demonstrate that NE induces ER stress by promoting ROS production in 16HBE14o‑airway epithelial cells, leading to increases in MUC5AC protein production and secretion via the IRE1α and XBP1 signaling pathways.The present study aimed to determine the anticancer effect of the herbal mixture extract C5E in the pancreatic cancer cell line, PANC‑1, in the absence or presence of gemcitabine treatment, a chemotherapeutic drug used for the treatment of pancreatic cancer. The anticancer effects of C5E, gemcitabine and C5E plus gemcitabine in PANC‑1 cells following 72 h of treatment were investigated. The effect of each treatment on cell cycle arrest, apoptosis and the proportion of side population (SP) cells was determined using flow cytometric analysis following propidium iodide (PI), Annexin V‑FITC/PI double staining and Hoechst 33342 staining, respectively. Bulevirtide supplier SP cells share similar characteristics to cancer stem‑like cells, and a reduction in the SP is considered to be indicative of an anticancer effect. The percentage of SP cells and the cell viability of general PANC‑1 cells were significantly decreased in response to all treatments. The percentage of SP cells was reduced from 8.2% (control) to 3.9, 7.2 and 5.1% following the treatment with C5E, gemcitabine and the co‑treatment, respectively. All three treatments were discovered to inhibit cell viability by arresting the cell cycle at the S phase and promoted cell death by inducing early apoptosis, with the levels of apoptosis being increased from 1.9% (control) to 7.3, 2.5 and 12.0% following the treatment with C5E, gemcitabine and the co‑treatment, respectively. The mRNA expression levels of sonic hedgehog, which is implicated in the development of certain types of cancer, were downregulated to a greater extent following the co‑treatment with C5E and gemcitabine compared with the treatment with either C5E or gemcitabine alone. As the co‑treatment with gemcitabine and C5E was more effective than each individual treatment, the present study suggested that the combined treatment may exhibit synergistic effects in PANC‑1 cells.Gastric cancer (GC) is a common malignant tumor in the digestive system, which presents without specific symptoms. Circular RNAs (circRNAs) play important roles in tumor progression and cellular functions; however, the relationship between GC and hsa_circ_0072309 remains unclear. The aim of the present study was to investigate the molecular mechanisms of hsa_circ_0072309 and the role that hsa_circ_0072309 plays in proliferation, invasion and migration of GC cells. The expression of hsa_circ_0072309 was evaluated using reverse transcription‑quantitative PCR. A series of functional experiments were performed to study the role that hsa_circ_0072309 has in survival and metastasis of GC cells. In the present study, hsa_circ_0072309 was downregulated in GC cell lines and its overexpression inhibited the proliferation, migration and invasion of GC cells. In addition, hsa_circ_0072309 overexpression induced activation of the peroxisome proliferator‑activated receptor γ (PPARγ)/PTEN pathway and inhibition of PI3K/AKT signaling. Moreover, pioglitazone, a PPARγ agonist, strengthened the effects of abundant hsa_circ_0072309 on the proliferative, migratory and invasive capabilities of GC cells, while GW9662, a PPARγ antagonist, abolished the effects of hsa_circ_0072309 overexpression on cell proliferation, migration and invasion. The present findings suggested that hsa_circ_0072309 inhibited proliferation, invasion and migration of gastric cancer cells via the inhibition of PI3K/AKT signaling by activating the PPARγ/PTEN signaling pathway. Targeting hsa_circ_0072309 may be an innovative therapeutic strategy for the treatment of GC.The transformation of vascular smooth muscle cells (VSMCs) into the proliferative migratory phenotype in the plaque area contributes to stable plaque formation and facilitates the pathogenesis of atherosclerosis. Stromal interaction molecule 1 (STIM1) has been identified to promote the proliferation of VSMCs, suggesting that STIM1 may be a potent target for the prevention and treatment of atherosclerosis. Bioinformatics analysis has previously predicted STIM1 as a target of microRNA (miR)‑541‑3p. The present study aimed to determine the effect of the miR‑541‑3p/STIM1 axis on the progression of atherosclerosis in vitro. Oxidized low‑density lipoprotein (ox‑LDL)‑treated VSMCs were used as an in vitro atherosclerosis model. Cell Counting Kit‑8 and Transwell migration assays were used to analyze cell viability and migration, respectively. Reverse transcription‑quantitative PCR and western blotting were applied to measure mRNA and protein expression levels, respectively. The association between miR‑541‑3p and STIM1 was detected using a dual luciferase gene reporter assay. The results of the present study revealed that ox‑LDL treatment significantly downregulated miR‑541‑3p expression levels and upregulated STIM1 expression levels in VSMCs. In addition, ox‑LDL stimulation enhanced cell viability and migration. The overexpression of miR‑541‑3p significantly reversed the ox‑LDL‑mediated increase in cell viability and migration, whereas the knockdown of miR‑541‑3p expression enhanced the ox‑LDL‑mediated effects. STIM1 was confirmed to be a target gene of miR‑541‑3p in VSMCs. The knockdown of STIM1 significantly impaired the stimulatory effects of miR‑541‑3p knockdown on cell viability and migration. In conclusion, the findings of the present study suggested that miR‑541‑3p may efficiently repress VSMC viability and migration by targeting STIM1 under the treatment of ox‑LDL. These results indicated that the miR‑541‑3p/STIM1 axis may represent a potent target to modulate VSMC viability and migration.