| Name |
BCL-xL
|
| Type |
gene
|
| Species |
Homo sapiens
|
| Tissue |
cell line (MDA-MB-231, HCC38, BT549, HCC1143, HCC70,; MDA-MB-468)
|
| Experiment Method |
PCR, Flow cytometry assay, RNAi, Western blot
|
| Up/Down |
Up
|
| Pro/Anti |
Pro
|
| Funtion Description |
Thus, in response to BETi, TNBC cells can either undergo apoptosis or survive through the activation of senescence.Cell lines that senesce and survive following BETi exposure express higher basal levels of BCL-xL.
|
| Regulation Gene |
NA
|
| Year |
2019
|
| Pubmed ID |
30482844
|
| Title |
Targeting BCL-xL improves the efficacy of bromodomain and extra-terminal protein inhibitors in triple-negative breast cancer by eliciting the death of senescent cells.
|
| Drug |
JQ1
|
| Disease |
triple-negativebreast cancer (TNBC)
|
| Environment Factors |
NA
|
| Circulating |
NA
|
| Variant |
NA
|
| High-throughput |
NA
|