Furthermore, restoring KDM7A and BCL2 expression rescued apoptosis inhibition in breast cancer, suggesting that KDM7A inhibited apoptosis by upregulating the BCL2 level in breast cancer.
The results indicated that MVs have a size range of 500-1500 nm, and the viability of MCF-7 was significantly decreased when treated by different concentrations of MVs and it was confirmed when apoptosis-related genes' expression level was measured by real-time reverse transcription polymerase chain reaction whereas demonstrated that apoptosis genes including Bax, P53, P21, and EP300 (2<sup>- ΔΔ CT</sup>) and ΔCT values were expressed significantly in MCF-7 treated by MVs higher than those nontreated, and decrease of Bcl-2 expression level in MVs-treated MCF-7 was also significant as an antiapoptosis-related gene.
The secondary metabolites produced by Lactobacillus plantarum downregulate BCL-2 and BUFFY genes on breast cancer cell line and model organism Drosophila melanogaster: molecular docking approach.
Potentiating apoptosis and modulation of p53, Bcl2, and Bax by a novel chrysin ruthenium complex for effective chemotherapeutic efficacy against breast cancer.
Upregulation of IQGAP3 inhibited apoptosis in BC cells, along with increased expression of phosphorylated extracellular signal-regulated kinases 1/2 (p-ERK1/2) and B cell lymphoma 2 (Bcl2) and decreased Bcl-2-associated X protein (Bax) expression, which was counteracted by Kaempferol treatment.
We demonstrate the translational potential of an AMPK and BCL-2/BCL-X<sub>L</sub> co-targeting strategy in ex vivo and in vivo models of MYC-high breast cancer.
We investigated the effect of amygdalin on the cell death and the level of pro-apoptotic Bax protein and anti-apoptotic Bcl-2 protein in SK-BR-3 human breast cancer cell line.
Bcl-2 overexpression is commonly associated with various cancers including breast cancer, prostate cancer, B-cell lymphomas and colorectal adenocarcinomas etc.
<i>Results:</i> The expression of miR-125a-5p in breast cancer cell lines, MDA-MB-157 cells, MDA-MB-361 cells and MDA-MB-415 cells, was significantly lower than that in normal breast epithelial cells, MCF-10A cells; The proliferation and invasion ability of MDA-MB-157 cells transfected with miR-125a-5p were significantly inhibited, and the apoptosis rate was significantly increased; Since GAB2 knocked down, the proliferation and invasion ability of MDA-MB-157 cells were significantly inhibited, while the apoptosis rate was significantly increased, the Bax protein expression was significantly down-regulated, and the Bcl-2 protein expression was significantly up-regulated; The dual-luciferase reporter assay demonstrated that miR-125a-5p can specifically target GAB2.
The results showed that ChPL inhibited breast cancer cell proliferation and induced apoptosis through the intrinsic pathway through down-regulation of anti-apoptotic Bcl-2 family proteins.
Moreover, qRT-PCR analysis revealed that Gemini-Cur could effectively upregulate the expression of p16INK4a, p14ARF and Bax, while significantly decreasing the Bcl-2 expression in these breast cancer cells.
The Bcl-2-associated death promoter BAD is a prognostic indicator for good clinical outcome of breast cancer patients; however, whether BAD affects breast cancer biology is unknown.
Therefore, we combined ITs (9.2.27-PE38KDEL or Mel-14-PE38KDEL) targeting chondroitin sulfate proteoglycan 4 (CSPG4) with a panel of Bcl-2 family inhibitors (ABT-737, ABT-263, ABT-199 [Venetoclax], A-1155463, and S63845) against patient-derived glioblastoma, melanoma, and breast cancer cells/cell lines.
Finally, we showed miR-106a overexpression upregulated the levels of Bcl-2 and ABCG2, and downregulated the expression of P53, Bax, and RUNX3. miR-106a promotes breast cancer cell proliferation and invasion through upregulation of Bcl-2, ABCG2, and P53, and downregulation of Bax and RUNX3.
In this issue, Lok and colleagues diverge from this paradigm by combining the BCL2 inhibitor venetoclax with tamoxifen in a phase Ib clinical trial, building on preclinical work to demonstrate that targeting apoptosis could represent a promising new strategy in the treatment of breast cancer.<i>See related article by Lok et al., p. 354</i>.
In conclusion, our results indicate that resveratrol acts as a potential inducer to enhance the chemosensitivity of breast cancer and also suggest that miR-122-5p is involved in the pathway of cell-cycle arrest by targeting Bcl-2 and CDKs.
Because anti-apoptotic BCL-2 family proteins can affect the threshold for induction of apoptosis and thus limit the effectiveness of the chemotherapeutic payload, we examined whether inhibition of BCL-2/X<sub>L</sub> would enhance the efficacy of T-DM1 in five HER2-expressing patient-derived breast cancer xenograft models.
The initial mechanism of MCZ-mediated cell death in human breast cancer MDA-MB-231 cells involves an increase in the Bax/Bcl-2 ratio, downregulation of apoptosis induced by Akt and p-Akt-473, a simultaneous upregulation of the receptor-interacting protein 3 (RIP3) and mixed lineage kinase domain-like (MLKL) protein expression, and ROS production to induce necroptosis.