In vitro, knockdown of CCAT2 enhanced radiosensitivity of EC cells and promoted apoptosis by increasing Bax/Bcl2 and active‑caspase 3/caspase 3 following X‑ray treatment.
In summary, shikonin can sensitize esophageal cancer cells to paclitaxel-treatment by promoting cell mitotic arrest and reinforcing the susceptibility of esophageal cancer cells to apoptosis induced by paclitaxel, which is potentially associated with altered levels of Bcl-2 and p53.
Zerumbone can inhibit the proliferation and induce apoptosis of esophageal cancer EC-109 cells, and its induction of apoptosis may be realized through upregulating the mRNA expression of P53 and downregulating the mRNA expression of Bcl-2, and upregulating the protein expression of P53 and downregulating the protein expression of Bcl-2.
In order to investigate the effect of recombinant GDF11 on the proliferation and apoptosis of esophageal cancer cells, the expression of apoptosis-promoting protein Bax and proliferative-associated protein Bcl-2 in esophageal cancer cells were determined using western blot.
These results suggest that targeting of the Bcl-2 family and P-gp is capable of reversing the resistance in EC109/PTX cells and the two-inhibitor combination may be a novel treatment strategy for resistant esophageal cancer.
In conclusion, Art exerted concentration-dependent inhibitory activity against esophageal cancer in vivo and in vitro by inducing cell apoptosis and cell cycle arrest through affecting mitochondrial membrane potential, BCL-2, Bax, caspase-3 and CDC25A.
PPSE inhibited the growth and proliferation on esophageal cancer ECA109 cells, while increasing the expression of connexin26 mRNA and protein; conversely, PPSE decreased Bcl-2 and increased Bad.
This study investigated the effect of ALA-PDT on esophageal squamous carcinoma cell line Eca-109 in vitro and vivo to explore optimal parameters, and evaluated the significance of cell apoptosis, cell cycle, ALA-protoporphyrin IX (ALA-PpIX) subcellular localization, and expression of Bcl-2 and Bax mRNA in cells to understand the mechanism of ALA-PDT for esophageal cancer.
We found that compared to control cells, overexpression of PTEN significantly suppressed growth and induced apoptosis in esophageal cancer cell lines Eca-109 and TE-1 via downregulation of Bcl-2 expression and changes in cell-cycle progression.
The ala43ala genotype of BCL2 anti-apoptotic gene was significantly associated with risk of developing esophageal cancer (OR 2.1, 95%CI=1.0-4.4, P=0.03), more so in males (OR 2.6, 95%CI=P=0.03).
Paraffin-embedded material from 37 patients with early esophageal cancer treated with PDT (argon dye laser after intravenous injection of hematoporphyrine derivative) was studied immunohistochemically for p53 protein nuclear accumulation and bcl-2 cytoplasmic expression.
These results indicate that the sensitivity of esophageal cancer cells to E2F-1-mediated apoptosis may be related to differential expression of Bcl-2 family member proteins and suggest that the adenovirus-mediated E2F-1 gene therapy may be a promising treatment strategy for the treatment of this disease.
Thus, bcl-2-protein is frequently expressed in invasive squamous-cell carcinomas of the esophagus and in precursor lesions of esophageal cancer, but has no significant impact on the outcome of esophageal cancer.