Apatinib strengthens the anti-tumor influence of cisplatin in thyroid carcinoma through VEGFR2-Akt-mTOR pathway.

Apatinib strengthens the anti-tumor influence of cisplatin in thyroid carcinoma through VEGFR2-Akt-mTOR pathway.

Head and neck squamous cell carcinoma (HNSCC) is a major malignancy worldwide. Ras overexpression in HNSCC is known to promote tumor cell growth; therefore, inhibition of Ras activation could lead to tumor growth suppression in HNSCC patients. Here, we investigated the effect of FTI-277, a farnesyl transferase inhibitor, and GGTI-287, a geranyltransferase 1 inhibitor, on the Ras signaling pathway in HNSCC cell lines-HEp-2 and HSC-3.

Cell viability was analyzed using the trypan blue staining exclusion assay. The apoptosis of cells was assessed by flow cytometry and caspase activation analysis. The expression levels of proteins were examined using western blot analysis.

FTI-277 and GGTI-287 induced cell death, enhanced caspase 3 activity, and increased the number of annexin V-positive cells in HEp-2 and HSC-3 cells. FTI-277 and GGTI-287 induced apoptosis in HSC-3 cells at much lower concentrations than that in HEp-2 cells. FTI-277 and GGTI-287 decreased the concentration of phosphorylated ERK1/2 and mTOR via membrane localization of Ras and enhanced Bim expression. Furthermore, FTI-277 and GGTI-287 induced cell death in v-H-Ras-transfected NIH3T3 (NW7) cells and not in empty vector-transfected NIH3T3 (NV20) cells.

FTI-277 and GGTI-287 may be useful as potential therapeutic agents for treating HNSCC patients; moreover, farnesyl transferase and geranylgeranyltransferase 1 inhibitors can be further developed as anticancer agents.

FTI-277 and GGTI-287 may be useful as potential therapeutic agents for treating HNSCC patients; moreover, farnesyl transferase and geranylgeranyltransferase 1 inhibitors can be further developed as anticancer agents.

The purpose of this study was to observe the effects of micro ribonucleic acid (miR)-505-5p on the proliferation and apoptosis of osteosarcoma cells, and to further investigate its potential mechanism.

Human osteosarcoma U2-OS cell lines were divided into Control group, miR-505-5p nonsense sequence (NS) group and miR-505-5p inhibitor group. Subsequently, cell proliferation and apoptosis in each group were observed. Finally, the effect of miR-505-5p on the in vivo growth of osteosarcoma was explored by means of subcutaneous tumor formation assay.

The expression of miR-505-5p in the cancer tissues was remarkably higher than in normal paracancer tissues of osteosarcoma patients. U2-OS cell lines cultured in vitro in miR-505-5p inhibitor group manifested notably weakened proliferative ability after transfection with miR-505-5p inhibitor. Colony formation assay showed that the number of colonies formed in miR-505-5p inhibitor group was obviously smaller than that in Control group. selleck The results of Western blotting assay indicated that the inhibition of miR-505-5p markedly increased the expression of Bax and decreased Bcl-2 in cancer cells (p<0.05). Furthermore, it was revealed that the inhibited miR-505-5p could distinctly up-regulate the protein expression level of RASSF8 in cancer cells. Furthermore, the miR-505-5p inhibition was able to prominently repress the subcutaneous tumor formation ability of osteosarcoma cells.

The expression level of miR-505-5p is raised significantly in the cancer tissues of osteosarcoma patients, and the inhibition of miR-505-5p can up-regulate RASSF8 to suppress the proliferation and promote the apoptosis of osteosarcoma cells.

The expression level of miR-505-5p is raised significantly in the cancer tissues of osteosarcoma patients, and the inhibition of miR-505-5p can up-regulate RASSF8 to suppress the proliferation and promote the apoptosis of osteosarcoma cells.

To detect the plasma levels of PLAC1 in osteosarcoma patients, and its regulatory effect on cell proliferation and apoptosis of osteosarcoma.

Plasma levels of PLAC1 in osteosarcoma patients were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Receiver operating characteristics (ROC) and Kaplan-Meier curves were performed for assessing the diagnostic and prognostic potentials of PLAC1 in osteosarcoma, respectively. Moreover, the regulatory effects of PLAC1 on proliferative and apoptotic rates of osteosarcoma cells were determined through cell counting kit-8 (CCK-8) and flow cytometry, respectively.

PLAC1 was highly expressed in plasma of osteosarcoma patients showing diagnostic and prognostic potentials. Overexpression of PLAC1 in U2-OS cells increased the proliferative rate but decreased the apoptotic rate, while knockdown of PLAC1 yielded the opposite results.

PLAC1 is upregulated in the plasma of osteosarcoma patients, serving as a diagnostic biomarker, and is unfavorable to the prognosis if this disease. PLAC1 promotes the development of osteosarcoma by stimulating cell proliferation and inhibiting apoptosis.

PLAC1 is upregulated in the plasma of osteosarcoma patients, serving as a diagnostic biomarker, and is unfavorable to the prognosis if this disease. PLAC1 promotes the development of osteosarcoma by stimulating cell proliferation and inhibiting apoptosis.

Gene polymorphism has a potential influence cancer susceptibility. This study aimed to explore the role of lncRNA H19 rs2839698 polymorphism and its genotypes in influencing NK/T cell lymphoma (NKTCL) in Chinese population.

NKTCL patients (n=573) and healthy participants (n=688) were recruited. Their blood samples were collected for detecting H19 rs2839698 polymorphism and its genotypes using PCR-RFLP. The correlations of H19 rs2839698 polymorphism with NKTCL susceptibility and pathological indexes were analyzed by logistic regression analysis.

No significant differences in age, body mass index (BMI), smoking, drinking and family history of cancer were detected between NKTCL patients and healthy participants. Hypertension and diabetes were statistically significant between groups. H19 rs2839698 polymorphism and its genotypes were correlated with NKTCL susceptibility. Moreover, compared with NKTCL patients carrying GG allele, patients carrying AG, AA and AG+AA alleles had more advanced tumor stage and higher incidence of EBV(+) and original involvement of non-paranasal structure.