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Potential function of LINC00460 in the progression of ovarian cancer (OC) and its underlying mechanism were studied. LINC00460 level in OC tissues and normal ovarian tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Correlation between LINC00460 level with tumor stage, tumor size and pathological subtypes of OC was analyzed. Potential influence of LINC00460 on proliferative ability and cell cycle progression was evaluated. In vivo tumorigenesis model was conducted by administration of A2780 cells transfected with sh-NC or sh-LINC00460 in nude mice. Predicted through JASPAR database, ZNF703 was screened out as the transcriptional factor binding to LINC00460 promoter region. Chromatin immunoprecipitation (ChIP) assay was performed to verify the binding relationship between ZNF703 and LINC00460. The potential role of ZNF703 in LINC00460-mediated OC progression was examined. LINC00460 was upregulated in OC tissues and cell lines. Its level increased with the deterioration of tumor stage and enlargement of tumor size. LINC00460 was highly expressed in serous ovarian cancer relative to other subtypes of OC. Knockdown of LINC00460 attenuated proliferative ability and arrested cell cycle of A2780 and HO8910 cells. ZNF703 was upregulated in OC tissues. ChIP assay showed pronounced enrichment of LINC00460 in ZNF703. Rescue experiments revealed that ZNF703 overexpression reversed the regulatory effects of LINC00460 on cellular behavior of OC cells. LINC00460 is upregulated in OC tissues and cell lines, which is closely related to tumor progression. It accelerates proliferative ability and cell cycle progression of OC cells via interacting with ZNF703.

The present study aimed to investigate the involvement of the recently identified long non-coding RNA neighboring enhancer of FOXA2 (lncRNA NEF) in laryngeal squamous cell carcinoma (LSCC). In this study, the expression levels of lncRNA NEF in tumor tissues and paired adjacent normal tissues were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Serum levels of NEF in patients with LSCC and healthy controls were also measured using RT-qPCR. Clinical and follow-up data of patients with LSCC were retrospectively analyzed. Diagnostic and prognostic values of serum NEF were evaluated by receiver operating characteristic curve and survival curve analysis, respectively. In addition, a NEF expression vector was constructed and transfected into human LSCC cells. The effects of NEF overexpression on cell proliferation, apoptosis and β-catenin expression were explored by Cell Counting kit-8 cell proliferation assay, MTT assay and western blotting. NEF was significantly downregulated in tumor tissues compared with in paired adjacent normal tissues of patients with LSCC. Serum levels of NEF were significantly lower in patients with LSCC than in healthy controls. Low serum levels of NEF distinguished patients with LSCC from healthy controls, and also indicated shorter postoperative survival. NEF overexpression inhibited proliferation and promoted apoptosis of LSCC cells, and also downregulated β-catenin expression. No significant effects of Wnt agonist on NEF expression were identified; however, Wnt agonist reduced the effects of NEF overexpression on cancer cell proliferation and apoptosis. In conclusion, lncRNA NEF may inhibit proliferation and promote apoptosis of LSCC cells by inhibiting Wnt/β-catenin signaling.

This study explored the target of miR-205 and the effect of miR-205 on the proliferation and migration regulating its target in thyroid cancer cells (TC). Twenty-five pairs of TC and adjacent tissues were collected after surgical resection. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression of miR-205 in TC tissues and cells (SW579, B-CPAP, TPC-1, WRO). SW579 cells were transfected with miR-205 mimic, and SW579 cells with overexpression of miR-205 were constructed. The effects of miR-205 overexpression on the proliferation and migration of SW579 cells were observed by cell counting kit-8 (CCK-8) and Transwell assays, respectively. Luciferase reporter assay was further used to look for the target of miR-205 and to study the mechanism of miR-205 in the proliferation and migration of TC cells. Compared with normal tissues and cells, the expression of miR-205 was significantly reduced in TC tissues (t=3.47, P=0.031) and cells (t=5.41, P=0.016). Overexpression of miR-205 inhibited the proliferation (t=4.12, P=0.035) and migration (t=4.47, P=0.027) of SW579 cells. Luciferase reporter assays found that CCNB2 was a target gene of miR-205 (t=4.63, P=0.024), qRT-PCR and western blot assays confirmed there was negatively correlation between CCNB2 and miR-205 (t=3.55, P=0.029; t=2.86, P=0.043). CCNB2 overexpression reversed the inhibition of miR-205 on the proliferation (t=3.70, P=0.031) and migration (t=4.12, P=0.022) of SW579 cells. In conclusion, miR-205 inhibits the proliferation and migration of TC cells by targeting CCNB2, which may be a potential target of TC therapy.

Glioblastoma is the most common primary brain carcinoma and leads to a poor survival rate of patients worldwide. Results of previous studies have suggested that tunicamycin may inhibit aggressiveness by promoting apoptosis of glioblastoma cells. In the present study, the effects of tunicamycin and its potential molecular mechanisms underlying the viability and aggressiveness of glioblastoma cells were investigated. Western blot analysis, the reverse transcription-quantitative polymerase chain reaction, immunohistochemistry, apoptosis assays and immunofluorescence were employed to examine the effects of tunicamycin on apoptosis, viability, aggressiveness and cell cycle arrest of glioblastoma cells by downregulation of the expression levels of fibronectin and epithelial cadherin. In vitro experiments demonstrated that tunicamycin significantly inhibited the viability, migration and invasion of glioblastoma cells. Results demonstrated that tunicamycin administration promoted apoptosis of glioblastoma cells through the upregulation of poly(ADP-ribose) polymerase and caspase-9. Cell cycle assays revealed that tunicamycin suppressed the proliferation of, and induced cell cycle arrest at S phase in, glioblastoma cells. Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/β-catenin in glioblastoma cells. Results also indicated that tunicamycin administration promoted the Wnt/β-catenin signaling pathway in glioblastoma cells. Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/β-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma. In vivo assays demonstrated that tunicamycin treatment significantly inhibited tumor viability and promoted apoptosis, which further led to an increased survival rate of tumor-bearing mice compared with that of the control group. In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/β-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy.

The aim of the present study was to examine the effectiveness of curcumin and quercetin in modulating ultrastructural changes during lung carcinogenesis. A total of 24 male laka mice were divided into the normal control, benzo[a]pyrene (BP)-treated, BP+curcumin-treated, BP+quercetin- treated, and BP+curcumin+quercetin-treated groups (n=6 per group). Lung carcinogenesis was induced by a single intraperitoneal injection of BP [100 mg/kg of body weight (b.wt.)]. Curcumin was supplemented to mice at a dose level of 60 mg/kg of b.wt. in drinking water and quercetin was given at a dose level of 40 mg/kg of b.wt. in drinking water. The ultrastructure of BP-treated mice revealed disruptions in cellular integrity together with nuclear deformation and premature mitochondrial aging. Notably, supplementation with phytochemicals individually resulted in improvement of the ultra-histoarchitecture of BP-treated mice although the improvement was much greater with combined supplementation of phytochemicals. Furthermore, BP treatment revealed alterations in lung histoarchitecture, which, however, were improved appreciably following combined supplementation with curcumin and quercetin. The results of the present study show that, combined supplementation with curcumin and quercetin effectively preserved the histoarchitecture as well as ultra-histoarchitecture during BP-induced lung carcinogenesis in mice.

The present study aimed to investigate the potential anticancer effect and mechanisms of salvianolic acid B on osteosarcoma. Salvianolic acid B suppressed osteosarcoma cell proliferation and induced apoptosis in the osteosarcoma MG63 cell line, and activated the expressions of cleaved caspase-3, phosphorylated-tumor protein (p)38 mitogen-activated protein kinase (p-p38 MAPK) and phosphorylated-p53 (p-p53) proteins in the MG63 cells. Additionally, Salvianolic acid B also increased the level of reactive oxygen species (ROS) generation in the MG63 cells. The silencing of p38 expression inhibited the anticancer effect of salvianolic acid B on the levels of cell proliferation, p-p53 protein expression and ROS generation level in the MG63 cells. All these data supported the hypothesis that the anticancer effect of salvianolic acid B includes the suppression of cell proliferation and induces apoptosis in MG63 cells, and that p38 is important in the anticancer effect of salvianolic acid B on osteosarcoma cells due to the direct regulation of ROS generation. These data suggest that salvianolic acid B is important in the proliferation of osteosarcoma cells due to the direct regulation of p38-mediated ROS signaling.

The aim of the present study was to investigate the indirubin-enhanced effects of arsenic disulfide (As2S2) on the proliferation and apoptosis of diffuse large B-cell lymphoma (DLBCL) cells in order to identify an optimum combination therapy. The human DLBCL cells, LY1 and LY8, were treated with different concentrations of indirubin for 24, 48 and 72 h. Next, the cells were treated with 10 μM As2S2 or a combination of 10 μM As2S2 and 20 μM indirubin for 48 h. Cell proliferation inhibition was detected using cell counting kit-8 and cell apoptosis was determined using flow cytometry. The expression levels of Bcl-2, Bcl-2-associated X protein (Bax) and caspase-3 were analyzed by quantitative polymerase chain reaction (qPCR) and western blotting. The DLBCL cell viability exhibited no significant changes at 24, 48 or 72 h with increasing indirubin concentration. In addition, the apoptotic rates of the LY1 and LY8 cells demonstrated no noticeable effects at 48 h with increasing indirubin concentration. Following treatment with the combination of indirubin and As2S2, the inhibitory and apoptotic rates of the cells were notably increased compared with those of the As2S2-treated group. The qPCR results revealed that indirubin alone had no enhancing effect upon the Bax/Bcl-2 mRNA expression ratio and caspase-3 mRNA expression. Western blot analysis revealed that indirubin alone had an enhancing effect upon the Bax/Bcl-2 protein ratio and procaspase-3 protein expression. In addition, the results demonstrated that the 21-KDa Bax protein was proteolytically cleaved into an 18-KDa Bax in the DLBCL cells treated with the combination of indirubin and As2S2. Indirubin alone did not inhibit proliferation or induce the apoptosis of the LY1 and LY8 cells. However, the combination of indirubin and As2S2 yielded enhancing effects. Therefore, the results of the present study demonstrated that with regard to antitumor activities, As2S2 served as the principal drug, whereas indirubin served as the adjuvant drug. The enhancing effect was due, in part, to the induction of the mitochondrial apoptotic pathway, which involves the cleavage of Bax.

Traditional Chinese medicine (TCM) has been demonstrated to have potent cytotoxic activity against certain malignant tumors. Ionizing radiation (IR) is one of the most effective methods used in the clinical treatment of cancer. The drawback of a single formula is that it limits the treatment efficacy for cancer, while comprehensive strategies require additional theoretical support. However, a combination of different antitumor treatment modalities is advantageous in restricting the non-specific toxicity often observed with an extremely high dose of a single regimen. The induction of apoptotic cell death is a significant process in tumor cells following radiotherapy or chemotherapy, and resistance to these treatments has been linked to a low propensity for apoptosis. Autophagy is a response of cancer cells to IR or chemotherapy, and involves the prominent formation of autophagic vacuoles in the cytoplasm. In this review, the synergistic effects of TCM and radiotherapy are summarized and the underlying mechanisms are illustrated, providing new therapeutic strategies for cancer.