B-cell lymphoma/leukemia gene-2 (Bcl-2) is the primary proto-oncogene that has been shown to work by preventing apoptosis/programmed cell death. Bcl-2 combines a variety of cell-generated signals associated to the survival and death of cells. In glioma, lung, and breast cancer, Bcl-2 over-expression has been linked to an increase in invasion and migration. Many treatment regimens that target Bcl2 have been established and approved, and thus increasing the survival rates of the patients. The primary goal of this research was to recognize new therapeutic compounds that target Bcl2 and assess Bcl2 expression pattern in BC patients. We used various bioinformatic tools as well as several in vitro assays to look out the expression and inhibition of Bcl2 in BC. Our study depicted that Bcl2 had a strong connection with tumour stroma, notably with suppressor cells originating from myeloid tissues. Moreover, in vitro and in silico research identified Paclitaxel as a promising natural substance that targets Bcl2. Overall, this work shows that Bcl2 overexpression accelerates the development of BC, and that targeting Bcl2 in combination with other drugs will dramatically improve BC patient's response to treatment and prevent the emergence of drug resistance.

Background: B-cell lymphoma/leukemia gene-2 (Bcl-2) is the first proto-oncogene that has been shown to work by preventing apoptosis/programmed cell death. Bcl-2 combines a variety of cell-generated signals associated to the survival and death of cells. In glioma, lung, and breast cancer, Bcl-2 overexpression has been linked to an increase in invasion and migration. Many treatment regimens that target BCL2 have been established and approved, and thus increasing the survival rates of the patients. Aim: The primary goal of this research was to identify new therapeutic compounds that target BCL2 and assess BCL2 expression pattern in BC patients. Methods: We used various bioinformatic tools as well as several in vitro assays to find out the expression and inhibition of Bcl2 in BC. Results: Our study shows that BCL2 had a strong connection with tumour stroma, notably with suppressor cells originating from myeloid tissues. Moreover, in vitro and in silico research identified Paclitaxel as a promising natural substance that targets BCL2. Conclusion: Overall, this work shows that BCL2 overexpression accelerates the development of BC, and that targeting BCL2 in combination with other therapeutic drugs will dramatically improve BC patients' responses to therapy and prevent the emergence of chemoresistance.