Search

Immunotherapy is a promising anticancer strategy. In the present report, the case of a 36-year-old female patient with pathologically diagnosed, left triple-negative breast cancer and axillary lymph node involvement is reported. The patient received immunotherapy in combination with neoadjuvant anthracycline-free chemotherapy for six cycles, before undergoing left mastectomy and left axillary lymph node dissection. The postoperative pathology was a complete response to treatment, involving eradication of tumor from both the breast and the relevant lymph nodes. However, thyroid dysfunction occurred after two cycles of neoadjuvant treatment. The clinical presentation of the thyroid disorder was transient hyperthyroidism for 4 weeks and subsequent hypothyroidism, which required hormone replacement therapy. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effect of dihydroartemisinin (DHA) on a multiple myeloma cell line. An MTT assay, flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) were used for the analysis of cell viability, cell cycle distribution and c-Jun N-terminal kinase (JNK) expression, respectively. Treatment of U266 cells using DHA caused a significant (P<0.05) decrease in cell viability compared with the control cells. An increase in the concentration of DHA from 1 to 100 μmol/l reduced cell viability from 87 to 35% compared with 100% in the control cultures at 48 h. A significant (P<0.05) increase was observed in the sub-G0/G1 phase population of the U266 cells with an increase in DHA concentration from 1 to 100 μmol/l. Treatment with 1, 3, 10, 30 and 100 μmol/l concentrations of DHA increased the sub-G0/G1 phase cell population to 3.13, 8.25, 24.91, 31.47 and 38.54%, respectively. RT-PCR analysis of DHA-treated or -untreated U266 cells after 48 h demonstrated a significant (P<0.01) increase in caspase-3 expression. Treatment of the cells for 48 h with DHA led to a significant increase in c-Jun expression. DHA treatment at 1, 3, 10, 30 and 100 μmol/l concentrations caused an increase in the level of c-Jun by 0.174±0.001, 0.254±0.002, 0.387±0.001, 0.502±0.003 and 0.679±0.005, respectively, compared with 0.982±0.001 in the control cells. The addition of SP600125 to the cells incubated with DHA resulted in a significant decrease in the caspase-3 and c-Jun expression levels compared with those cells incubated with DHA alone. These findings confirm that treatment with DHA increased caspase-3 and c-Jun expression in the U266 cells through activation of the JNK signaling pathway. Thus, DHA inhibited proliferation of multiple myeloma cells by interfering with the JNK signaling pathway. [ABSTRACT FROM AUTHOR]

Nerve growth factor (NGF), a prototypical neurotrophic factor essential for neuronal cell proliferation and survival, has been implicated as a marker of tumor progression, as well as a potential target for novel therapeutic approaches in cancer. To investigate the functional potential of NGF in liver cancer in the present study, a stable NGF-overexpressing HepG2 cell line was generated. The scratch-wound assay was used to investigate cell motility and polarity. Western blotting was performed to evaluate the expression levels of epithelial-mesenchymal transition (EMT)-related proteins, including E-cadherin, N-cadherin and vimentin. Moreover, immunofluorescence was performed to investigate the arrangement of the actin cytoskeleton. Cell anoikis resistance was examined using a suspension culture model and cell apoptosis was examined via flow cytometry. The present results indicated that NGF overexpression in HepG2 cells disrupted HepG2 cell polarity and promoted cell motility. Furthermore, NGF overexpression induced EMT and actin cytoskeleton rearrangement in HepG2 cells, as well as enhanced anoikis resistance and prevented cellular apoptosis. Notably, a tropomyosin receptor kinase A receptor inhibitor blocked NGF-induced cell motility and apoptosis. Therefore, it was suggested that NGF serves a critical role in the invasion and metastasis of liver cancer. The use of NGF as a biomarker or potential new target could lead to the development of novel factors for diagnosis or for improving therapeutic strategies in liver cancer. [ABSTRACT FROM AUTHOR]