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However, the low concentration statin‑induced gene expression alterations were only detected in MiaPaCa2 cells. In conclusion, a marked difference in the intra and inter cell‑type performance of pancreatic cancer cells exposed to a variety of statins at low or high concentrations was reported herein, which may provide insights for the potential clinical use of statins in future pancreatic cancer therapeutics.Osteosarcoma is the most common primary malignant bone tumor in children and adolescents and its long‑term survival rate has stagnated in the past decades. Previous studies have shown that tumors in the G2/M phase are more sensitive to radiotherapy. The proto‑oncogene c‑myc is a transformed member of the myc family and c‑myc‑interacting zinc finger protein‑1 (Miz‑1) is a poly‑Cys2His2 zinc finger (ZF) activator of cell cycle regulator genes, such as the cyclin‑dependent kinase inhibitor p21. C‑myc can repress the expression of p21 by binding to Miz‑1 and abolishing the interaction between Miz‑1 and its co‑activators, which induces G2/M phase arrest. Therefore, the present study investigated the radiosensitizing effects of the c‑myc gene and the sensitizing apoptosis pathway, aiming to identify a more effective combination radiotherapy treatment for osteosarcoma. The present study demonstrated that the c‑myc gene was overexpressed in osteosarcoma cells compared to osteoblasts. Following inhibition of c‑myc gene expression in osteosarcoma cells, tumor proliferation was significantly hindered after inducing G2/M phase arrest via regulating G2/M phase‑associated proteins. Additionally, it was revealed that inhibiting c‑myc gene expression combined with radiotherapy could significantly increase the apoptosis rate of osteosarcoma cells via the mitochondrial signaling pathway. In summary, the present study verified the radiosensitizing effects of c‑myc gene knockdown‑induced G2/M phase arrest, which was achieved by intrinsic stimuli through the mitochondrial signaling pathway.Poncirus fructus (PF) is a phytochemical compound extracted from the dry, immature fruits of Poncirus trifoliate. PF is traditionally used to treat gastrointestinal disorders, allergies, and inflammatory disease. In East Asia, PF is also known for its anticancer properties. There are numerous reports on the anticancer and anti‑inflammatory effects of PF in a wide range of cancers and gastrointestinal diseases, respectively. However, the role of PF in inducing apoptosis and suppressing the invasiveness of hepatocellular carcinoma (HCC) remains unclear. This study investigated the ability of PF to induce apoptosis and inhibit the invasiveness and migratory ability of HCC cell lines (Hep3B and Huh7). Wound healing, Transwell migration and invasion, and colony‑formation assays, as well as flow cytometry, were used to analyze cell proliferation, migration, invasion, and apoptosis. Epithelial‑mesenchymal transition (EMT)‑related and apoptotic proteins were assessed by western blotting. #link# The mitochondrial membrane potential of the Hep3B and Huh7 cells was observed with tetramethylrhodamine ethyl ester. The reactive oxygen species (ROS) level was determined by dihydroethidium (DHE) staining. PF treatment significantly decreased the proliferation of Hep3B and Huh7 cells in a dose‑dependent manner, reduced the mitochondrial membrane potential, increased ROS levels, decreased the protein levels of Bcl‑2, and increased the protein levels of Bax and cleaved caspase‑3 and 9, suggesting that PF mediated HCC apoptosis via a mitochondrial pathway. Our findings showed that PF prevented HCC cell migration and invasion by inhibiting the EMT process and downregulating MMP‑2 and MMP‑9 activities. The results suggest the potential anticancer effects of PF by inhibiting proliferation, inducing apoptosis, and reducing the invasion and migration of HCC cells.Thyroid cancer (TC) is one of the most common malignancies with a high mortality rate. Long non‑coding RNA CCAT2 (CCAT2) participates in the occurrence and development of certain human cancers; however, whether it is involved in TC remains unclear. Thus, the present study investigated the role of CCAT2 in TC and the underlying mechanism. CCAT2 expression in both TC tissues and cell lines was examined by reverse transcription‑quantitative PCR. CCAT2 expression was silenced in TC cell lines by a specific small interfering (si)RNA against CCAT2 (si‑CCAT2). GW441756 of CCAT2 silencing on TC cell proliferation were detected by CCK‑8 and colony formation assays. link2 Cell cycle and apoptosis of the treated TC cells were assessed by flow cytometry. Wound healing and Transwell assays were performed to detect the effects of si‑CCAT2 on the migration and invasion of TC cells. Apoptosis‑related proteins and Wnt/β‑catenin cascade‑associated agents were examined by western blotting. The interaction between CCAT2 and the Wnt/β‑catenin pathway in the transfected cells was detected by performing a dual‑luciferase reporter assay. CCAT2 expression was increased in TC tissue samples and cell lines compared with the controls. Tissue CCAT2 level was associated with T stage and tumor‑node‑metastasis stage of TC. Silencing CCAT2 inhibited TC cell proliferation, migration and invasion, and promoted TC cell cycle arrest and apoptosis. Furthermore, CCAT2 knockdown suppressed the activity of the Wnt/β‑catenin cascade in TC cells treated with lithium chloride. In summary, the present study demonstrated that CCAT2 knockdown suppresses TC progression via inactivating the Wnt/β‑catenin cascade, indicating that suppressing CCAT2 and the Wnt/β‑catenin signaling pathway may be a promising therapeutic strategy for treating TC.Recent studies have reported that filamin A (FLNa) and uncoupling protein 2 (UCP2) are highly expressed in various types of cancer, but little is currently known about their roles in cervical cancer (CC). In the present study, immunohistochemical staining of paraffin sections of cervical tissues was performed in order to compare the differential expression of FLNa, UCP2, p16 and Ki67 between CC and high‑grade intraepithelial neoplasia (HSIL). UCP2 and FLNa were knocked down in CC cell lines to investigate the effects on cell proliferation, cell cycle arrest, apoptosis, migration and invasion. In addition, the present study investigated the expression of cell‑associated proteins [extracellular signal‑regulated kinase (ERK), phosphorylated (p) ERK, protein kinase B (AKT), p‑AKT and B‑cell lymphoma‑2 (Bcl‑2)] and the mRNA levels of cellular proteins such as Ras, matrix metalloproteinase (MMP)‑2 and MMP‑9. FLNa and UCP2 expression levels were significantly higher in CC tissues than in HSIL tissues, with no significant differential expression of p16 or Ki67. UCP2 expression was significantly different in patients with clinical stage II or higher or lymph node metastasis compared with in other patients with cervical cancer. FLNa or UCP2 knockdown slowed or decreased SiHa and HeLa cell proliferation, migration and invasion, with no significant change in apoptosis, and downregulated the protein levels of p‑ERK1/2, and the mRNA levels of Ras, MMP‑2 and MMP‑9. UCP2 knockdown arrested the cell cycle at the G2 phase in SiHa and HeLa cells, while FLNa knockdown arrested the cell cycle at the G2 phase in HeLa cells. The results of the present study revealed that FLNa and UCP2 play roles in the development and progression of CC via the Ras/MAPK/ERK signalling pathway. FLNa and UCP2 are superior to p16 and Ki67 for early prediction of CC, indicating that FLNa and UCP2 may be used for the early diagnosis of CC. UCP2 may be used to predict the prognosis of CC.Voltage‑dependent anion channel 1 (VDAC1) functions as a porin in the mitochondrial outer membrane (MOM) and plays important roles in mitochondria‑mediated cell apoptosis. VDAC1 interacts with a variety of proteins, such as Bcl‑2 family proteins, hexose kinase (HK), adenine nucleotide translocase (ANT) and α‑tubulin. However, the association between VDAC1 and α‑tubulin, particularly between VDAC1 and acetylated α‑tubulin (Ac‑α‑tubulin), in apoptosis remains unclear. The present study revealed that the heat shock protein 90 inhibitor, tanespimycin, induced VDAC1 upregulation and α‑tubulin acetylation during Calu‑1 cell apoptosis in human lung cancer. Hsp90 mediated the expression level of VDAC1, and the acetylation of α‑tubulin was enhanced in an α‑tubulin acetyltransferase 1 (αTAT1)‑dependent manner following an increase in VDAC1 expression. Docetaxel, as an inhibitor of microtubules, augmented the expression of Ac‑α‑tubulin, VDAC1 and Bax induced by tanespimycin and increased the degree of caspase activation. Immunoprecipitation (IP) experiments revealed that Ac‑α‑tubulin, α‑tubulin and VDAC1 were co‑precipitated in the IP complex, in which α‑tubulin expression was decreased and VDAC1 proteins were oligomerized, and that the p‑AKT/glycogen synthase kinase 3β (GSK3β) signalling pathway mediated the opening of VDAC1. Therefore, it can be asserted that the acetylation of α‑tubulin and VDAC1 upregulation or oligomerization induced by tanespimycin may lead to mitochondrial permeability and consequently induce the apoptosis of lung cancer cells. These findings provide evidence for the use of a combination of drugs that target VDAC1 and tubulin to induce tumour cell apoptosis.The N‑glycoforms of glycoproteins modify protein function and control a number of biological pathways. The aim of the present study was to investigate the correlation between alterations in N‑glycans and cancer aggressiveness in terms of cancer cell invasion ability. The expression of urokinase‑type plasminogen activator (uPA) and N‑acetylglucosaminyltransferase V (GnT‑V) in liver cancer cell lines was analyzed by western blotting. Cell invasiveness was analyzed by Matrigel invasion assays. uPA and GnT‑V expression in liver cancer cell lines was knocked down by RNA interference. Furthermore, uPA was overexpressed in liver cancer cells using lentiviral vectors, and a mutant strain of HepG2 cells overexpressing uPA deficient in N‑glycans was established. A glycoblotting‑assisted matrix‑assisted laser desorption/ionization‑time‑of‑flight/mass spectrometry‑based quantitative analysis of liver cancer cell lines was performed, in which invasiveness was altered by modifying the expression of uPA and GnT‑V. N‑glycan profiles were found to differ between the highly invasive liver cancer cell line HLE and the less invasive cell line HepG2. The expression of several N‑glycans, including a form with m/z=1892, was changed according to invasiveness controlled by knockdown and overexpression of uPA. The invasiveness of HepG2 cells with mutant uPA did not increase regardless of the level of expression of uPA. Following GnT‑V knockdown and N‑glycan alteration, uPA expression did not change, whereas cell invasiveness decreased. One N‑glycan (m/z=1892) was common among N‑glycans in the comparative analysis between HLE and HepG2, HLE and uPA knockdown HLE, HepG2 and uPA‑overexpressing HepG2, and HLE and GnT‑V knockdown HLE cells and among N‑glycan profiles in human uPA. link3 Therefore, N‑glycosylation is an important factor controlling invasiveness of liver cancer cells, and a specific N‑glycan (m/z=1892) associated with the invasion of liver cancer cells via uPA was identified in the present study.
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