The expression levels of eight differentially expressed genes (NTRK2, DTNA, BTG2, COL11A1, Smad2, Smad4, PIK3R1, and BCL2) in The Cancer Genome Atlas database were compatible with our RNA-sequencing.
We examined Bcl-2 expression in 104 squamous cell carcinomas of the head and neck, as well as histologically normal mucosa several centimeters away from the tumor, and in control normal mucosa from patients without cancer.
All patients were treated by BOAI, and expression of cancer cell apoptosis was examined by the TUNEL method, expression of bax, bcl-2 and bcl-xL proteins were examined by immunohistochemistry, and expression of bax, bcl-2 and bcl-xL mRNA was examined by quantitative RT-PCR before and 3 days after BOAI.
Therefore, we performed this meta-analysis regarding the relationship between Bcl-2 promoter single nucleotide polymorphisms (SNPs) and cancer susceptibility and prognosis.
Design, synthesis and characterization of novel quinacrine analogs that preferentially kill cancer over non-cancer cells through the down-regulation of Bcl-2 and up-regulation of Bax and Bad.
Deregulated expression of anti-apoptotic BCL-2 can be a primary aberration that promotes malignancy and also confers resistance to chemotherapeutic agents.
Thus, BCL-2 has become an attractive target for therapeutic strategy in cancer, as demonstrated by the recent approval of ABT-199 (Venclexta™) in relapsed or refractory Chronic Lymphocytic Leukemia with 17p deletion.
Infection of Ad.PEG-E1A-mda-7 (CTV) in normal prostate epithelial cells and parental and Bcl-2- or Bcl-x(L)-overexpressing prostate cancer cells confirmed cancer cell-selective adenoviral replication, mda-7/IL-24 expression, growth inhibition, and apoptosis induction.
Small-molecule inhibitors that antagonize anti-apoptotic Bcl-2 proteins such as BH3 mimetics are currently considered as promising cancer therapeutics to engage the mitochondrial pathway of apoptosis in cancer cells.
Autophagy can be regulated by a limited number of autophagy-related genes (Atgs) such as oncogenic Bcl-2/Bcl-XL , mTORC1, Akt and PI3KCI, and tumour suppressive proteins PI3KCIII, Beclin-1, Bif-1, p53, DAPKs, PTEN and UVRAG, which play their crucial roles in regulating autophagy-related cancer.
Bcl-2 and Bax genes are probably involved in the reduction of malignancy of glioblastoma cell caused by the introduction of EGFR-antisense into these tumor cells.
These findings confirm that Bcl-2 is a pivotal target for cancer therapy and thus, further study of this novel combination of Bcl-2 reduction and angiogenic targeting in human tumors is warranted.