Analysis of thermochemotherapy-induced apoptosis and the protein expressions of Bcl-2 and Bax in maxillofacial squamous cell carcinomas

Abstract

The aim of this study is to investigate the relationship between thermochemotherapy-induced apoptosis and the expressions of the Bcl-2 and Bax proteins in maxillofacial squamous cell carcinomas. Fifteen patients with maxillofacial squamous cell carcinomas were treated with microwave hyperthermia (43 °C for 40 min) following the intravenous injection of pingyangmycin (Bleomycin A5 Hydrochloride for Injection) (8 mg). Subsequently, the tumors were surgically resected. The terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling method was used to assess the apoptosis in the carcinoma cells, and immunohistochemistry was performed using the streptavidin-peroxidase method to determine the expression levels of the Bcl-2 and Bax proteins, and quantitative analysis was employed. The number of apoptotic cells increased markedly (P < 0.001). The protein expression of Bcl-2 was downregulated (P < 0.001), while that of Bax was markedly upregulated (P < 0.001). Thermochemotherapy induces apoptosis in maxillofacial squamous cell carcinoma cells by downregulating the protein expression of Bcl-2 and upregulating that of Bax.

Correlation between the expression of Id-1 and hyperthermia-associated molecules in oral squamous cell carcinoma

“…In our study we found p-Akt and p-GSK3β overexpression in most of the tested oral cancer samples (65.8%, 60.5%), and the expression of p-Akt and p-GSK3β is correlated with advanced clinical stage, metastasis and recurrence. In our previous study,26 we found that the effect of thermochemotherapy was not correlated with gender, age, differentiation and advanced clinical stage.…”

Phosphoinositide 3-kinase/Akt pathway is involved in pingyangmycin-induced growth inhibition, apoptosis and reduction of invasive potential in EOMA mouse hemangioendothelioma cells

“…Yang et al (28) reported that PYM may induce apoptosis by activating c-Jun N-terminal kinases and inhibiting the activity of extracellular signal-regulated kinases 1 and -2 in KB cells. Zhao et al (25) reported that patients with maxillofacial squamous cell carcinomas subjected to microwave-induced hyperthermia followed by intravenous injection of PYM, exhibited an increased number of apoptotic cancer cells; this effect was likely to be mediated via downregulation of Bcl-2 and upregulation of Bax. In HemECs, the induction of apoptosis was attributed to the activation of the p53 pathway (24).…”

“…Originally, PYM was reported to exert its anti-cancer effects by DNA strand breaks (23). Recent studies have reported mechanisms including activation of the p53 pathway (24), downregulation of B-cell lymphoma 2 (Bcl-2) and upregulation of Bcl-2-associated X protein (Bax) (25) and induction of apoptosis by activation of caspase-3 (26) in vitro and in vivo, which may be downstream cellular responses to PYM treatment. The present study investigated the underlying mechanisms of the anti-cancer activity of PYM on hemangioma by examining its effects on cell viability, cell cycle, invasive potential and the expression of proteins involved in the angiogenesis-associated PI3K/Akt pathway using an MTT assay, flow cytometry, Transwell assay and western blot analysis.…”

Therapeutic mechanism of treating SMMC-7721 liver cancer cells with magnetic fluid hyperthermia using Fe2O3 nanoparticles

“…Regulation of apoptosis by the Bcl-2 and Bax genes, both of which are members of the Bcl-2 family, has increasingly become a research topic in molecular biology. Bcl-2 is antiapoptotic and its overexpression (Bcl-2-Bcl-2) results in apoptosis inhibition and cell survival, whereas Bax is proapoptotic (9,10), and its overexpression (Bax-Bax) leads to cell death. However, the expression of the apoptosis suppressor gene Bcl-2 is low or nonexistent in hepatoma cells (11,12), whereas Bax is widely distributed in various organs including normal liver tissues, which indicates that Bax is probably an important apoptosis-regulating gene (13).…”