Premium
Expression of the bcl ‐2 gene family in normal and malignant breast tissue: Low bax ‐α expression in tumor cells correlates with resistance towards apoptosis
Author(s) -
Bargou Railf C.,
Daniel Peter T.,
Mapara Markus Y.,
Bommert Kurt,
Wagener Christian,
Kallinich Bianca,
Royer Hans D.,
Dörken Bcrnd
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910600622
Subject(s) - apoptosis , cancer research , breast cancer , biology , programmed cell death , fas receptor , epithelium , cancer , cell culture , tumor suppressor gene , cell , pathology , carcinogenesis , medicine , genetics
We have studied the expression of the apoptosis‐regulating genes bcl‐2, bcl‐x, bax and APO‐1/fas (CD95) in human breast cancer. The expression pattern of these genes in human breast‐cancer tissues and breast‐cancer‐derived cell lines was compared to that seen in normal breast epithelium and breast epithelial cell lines. No difference with regard to bcl‐2 and bcl‐x L expression was observed between normal breast epithelium and tumor tissue or breast cancer and non‐malignant epithelial cell lines. In contrast, bax‐α, a splice variant of bax, which promotes apoptosis, is expressed in high amounts in normal cell lines and breast tissue, whereas only weak or no expression could be detected in cancer‐cell lines and malignant tissue. In contrast to malignant cell lines, which express low levels of bax‐α, non‐malignant epithelial cell lines displaying high amounts of bax‐α were highly sensitive to induction of programmed cell death by both serum starvation and APO‐1/fas (CD95) triggering. We therefore propose that dysregulation of apoptosis contributes to the pathogenesis of breast cancer, at least in part, due to an imbalance between anti‐apoptosis genes (such as bcl‐2/bcl‐x) and apoptosis‐promoting genes (bax).