Regulatory effect of Bcl-2 in ultraviolet radiation-induced apoptosis of the mouse crystalline lens

Abstract

The aim of the present study was to analyze the role of Bcl-2 during the process of apoptosis in the mouse crystalline lens. In total, 12 normal mice served as the control group and 12 Bcl-2 knockout (K.O) mice served as the experimental group. The mouse crystalline lens was sampled for the detection of Bcl-2 and caspase-3 expression following exposure to ultraviolet (UV) radiation. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine Bcl-2 expression in the groups of normal mice receiving UV radiation or not receiving UV radiation. Samples of the murine crystalline lens were microscopically harvested and analyzed using western blotting. Apoptosis was detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Furthermore, caspase 3 activity was examined using enzyme-linked immunosorbent assay kits, and RT-qPCR was used to analyze caspase-3 expression levels. The results of the present study demonstrated that there was no statistically significant difference in the level of Bcl-2 gene transcription between the two groups. In addition, UV radiation did not change the macrostructure of the crystalline lens in the group of normal mice or the group of Bcl-2 K.O mice. The results of the TUNEL assay indicated that the normal-UV group exhibited a more significant apoptosis level compared with the Bcl-2 K.O-UV group. Furthermore, the mRNA expression level of caspase-3 in the normal-UV group was significantly higher compared with the normal-nonUV group (P<0.05), while the levels in the Bcl-2 K.O-UV group were significantly higher compared with the Bcl-2 K.O and normal-nonUV groups (P<0.05). In addition, the mRNA expression level of caspase-3 was significantly higher in the normal-UV, as compared with the Bcl-2 K.O-UV group (P<0.05), and the variation trends in caspase-3 activity were consistent. In conclusion, the results of the present study demonstrated that Bcl-2 may have an important role in the promotion of UV-induced apoptosis in the crystalline lens.

Downregulation of TMPRSS4 Enhances Triple-Negative Breast Cancer Cell Radiosensitivity Through Cell Cycle and Cell Apoptosis Process Impairment

“…The pro-apoptotic protein (Bax and Caspase3) and the anti-apoptotic protein (Bcl2) are the kinds of the proteins related to cell apoptosis pathway and implicated in cancer radiotherapy (Mackey et al, 1998;Dong et al, 2016;Kaliberov et al, 2002). In the present study, we found that TMPRSS4 down-regulation improved the apoptosis effect of ionizing radiation on triple negative breast cancer ( Figure 4A, B) associated with inhibition of expression of Bcl2 and increased of Bax and Caspase3 ( Figure 4C).…”

N-myc downstream-regulated gene 1 promotes oxaliplatin-triggered apoptosis in colorectal cancer cells via enhancing the ubiquitination of Bcl-2

“…It was previously reported that the posttranscriptional modulation of Bcl-2, mainly through ubiquitination and phosphorylation, was responsible for its stability [ 46 , 47 ]. Bcl-2 was shown ubiquitinated and rapidly degraded in apoptosis trigged by TNF-α [ 48 ] and UV exposure [ 49 ]. Furthermore, attenuation of this ubiquitination process contributed to chemo-resistance in cancer cells.…”

Oridonin enhances the radiosensitivity of lung cancer cells by upregulating Bax and downregulating Bcl‑2

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