The in vitro study revealed that treatment with vismodegib decreased BCC cell growth and migration; however, these effects were reversed by LV‑CD44s overexpression. The in vivo study revealed that BCC tumour growth was significantly increased in nude mice transplanted with cells stably infected with CD44s compared with nude mice transplanted with cells infected with a control vector. Our investigation demonstrated that lentivirus‑mediated CD44s expression may reverse the effects of vismodegib treatment on BCC.Corosolic acid (CRA) is a pentacyclic triterpenoid isolated from Lagerstroemia speciosa. The aim of the present study was to determine whether CRA reduces cardiac remodelling following myocardial infarction (MI) and to elucidate the underlying mechanisms. C57BL/6J mice were randomly divided into control (PBS‑treated) or CRA‑treated groups. After 14 days of pre‑treatment, the mice were subjected to either sham surgery or permanent ligation of the left anterior descending artery. Following surgery, all animals were treated with PBS or CRA (10 or 20 mg/kg/day) for 4 weeks. After 4 weeks, echocardiographic, haemodynamic, gravimetric, histological and biochemical analyses were conducted. The results revealed that, upon MI, mice with CRA treatment exhibited decreased mortality rates, improved ventricular function and attenuated cardiac fibrosis compared with those in control mice. Furthermore, CRA treatment resulted in reduced oxidative stress, inflammation and apoptosis, as well as inhibited the transforming growth factor β1/Smad signalling pathway activation in cardiac tissue. In vitro studies further indicated that inhibition of AMP‑activated protein kinase α (AMPKα) reversed the protective effect of CRA. In conclusion, the study revealed that CRA attenuated MI‑induced cardiac fibrosis and dysfunction through modulation of inflammation and oxidative stress associated with AMPKα.The present study aimed to investigate the effects of electrical stimulation (ES) on cell activity, cell cycle and apoptosis in injured rat dorsal root ganglion (DRG) cells induced by cyclic mechanical stretching (CMS). The present study also investigated whether the Wnt/β‑catenin pathway is involved in this process. Injury and ES models were established in DRG cells. Then, cell activity was detected using a Cell Counting Kit‑8 and 5‑ethynyl‑2'‑deoxyuridine‑594 cell proliferation assay kit. Cell cycle distribution was detected using a cell cycle detection kit. Apoptosis was detected using an Annexin V‑FITC apoptosis detection kit, and Wnt/β‑catenin pathway‑associated proteins were detected using western blotting. The present study demonstrated that CMS decreased DRG cell activity, increased the number of cells in the S phase, promoted cell apoptosis and inhibited the Wnt/β‑catenin pathway. In addition, ES significantly increased the proliferation activity of DRG cells, increased the number of cells in the G2 phase, decreased the apoptotic rate and activated the Wnt/β‑catenin pathway, ultimately reversing the injury caused by CMS. Following inhibition of the Wnt/β‑catenin signaling pathway using XAV939, the effects of ES were weakened. Selleckchem Acetalax In conclusion, the present study demonstrated that ES may reverse CMS‑induced injury in DRG cells, and that the Wnt signaling pathway may be involved in this process.Glioma is the most commonly diagnosed primary intracranial malignant tumor with rapid growth, easy recurrence and thus poor prognosis. In the present study, the role of kinesin‑12 (KIF15) in glioma was revealed. Immunohistochemical staining and western blot analysis were used to detect the protein expression. An MTT assay was performed to evaluate cell proliferation. Flow cytometric analysis was utilized to assess cell apoptosis and the cell cycle. A mouse xenograft model was constructed for in vivo study. The results indicated that KIF15 was significantly upregulated in glioma tumor tissues and positively correlated with pathological staging, recurrence risk and poor prognosis. Silencing of KIF15 could inhibit cell proliferation and stemness of glioma cells, arrest cells in the G2 phase and induce cell apoptosis. The in vivo study verified the inhibitory effect of KIF15 knockdown on tumor growth. The mechanism study demonstrated the regulation of apoptosis‑ and cycle‑related proteins in the KIF15 KD‑induced inhibition of glioma. KIF15 was revealed to function as a tumor promoter in the development and progression of glioma. KIF15 also served as a prognostic indicator for glioma and may be a therapeutic target for glioma therapy.Cholesteatoma is a chronic disease that pathologically displays a benign tumor with excessive squamous epithelial cell proliferation in the middle ear. Clinically, however, it can manifest malignant behavior by destroying adjacent tissues and organs. Although previous studies have demonstrated that the pathogenesis of cholesteatoma is correlated with epigenetic dysregulation, the exact mechanism remains unclear. Circular RNAs (circRNAs) have been revealed as being abundantly expressed in various organisms and have been found to contribute to the regulation of many diseases. To date, no reports have elucidated their expression profiles and functions in cholesteatoma. In the present study, the circRNA expression profile in cholesteatoma was explored for the first time by using microarray analysis. We obtained a total of 355 significantly differentially expressed circRNAs in cholesteatoma, among which 101 were identified to be upregulated and 254 downregulated. By constructing circRNA‑lncRNA‑miRNA‑mRNA competing endogenous RNA (ceRNA) network, it was discovered that circRNAs may function as ceRNAs and contribute to the formation of cholesteatoma. These results provide novel insight into the pathogenesis of cholesteatoma and suggest circRNAs as potential promising therapeutic targets for cholesteatoma.Tumor angiogenesis is an important factor which precipitates recurrence and metastasis of colorectal cancer (CRC). Angiogenesis is also a significant feature which accompanies invasion and metastasis of CRC. Tumor hypoxia activates hypoxia inducible factor (HIF), which promotes angiogenesis in CRC. HIF significantly promotes cell proliferation and angiogenesis in CRC, facilitating invasion and metastasis. Tanshinone IIA (Tan IIA) has been revealed to effectively inhibit angiogenesis in CRC, although the underlying mechanism remains to be determined. The aim of the present study was to determine the effects of HIF‑1α on hypoxia induced angiogenesis in CRC cells, the effects of Tan IIA on the expression of pro‑angiogenic factors in CRC cells, and on human umbilical vein endothelial cell (HUVEC) tube formation in normal and hypoxic conditions. The results of the present study revealed that Tan IIA not only decreased HIF‑1α expression and inhibited the secretion level of vascular endothelial growth factor and basic fibroblast growth factor, but also efficiently decreased proliferation, tube formation and metastasis of HUVECs.