2019
DOI: 10.1371/journal.pcbi.1007485
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Alterations of the interactome of Bcl-2 proteins in breast cancer at the transcriptional, mutational and structural level

Abstract: Apoptosis is an essential defensive mechanism against tumorigenesis. Proteins of the B-cell lymphoma-2 (Bcl-2) family regulate programmed cell death by the mitochondrial apoptosis pathway. In response to intracellular stress, the apoptotic balance is governed by interactions of three distinct subgroups of proteins; the activator/sensitizer BH3 (Bcl-2 homology 3)-only proteins, the pro-survival, and the pro-apoptotic executioner proteins. Changes in expression levels, stability, and functional impairment of pro… Show more

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Cited by 50 publications
(48 citation statements)
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References 109 publications
(149 reference statements)
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“…As is shown in Figure 8, the direct results of PI3K phosphorylation is the phosphorylation of AKT, which further affects the expression of Bcl-2 and Bax proteins. Bcl-2 and Bax are a group of proteins closely related to mitochondrial mediated apoptosis, among which the antiapoptotic protein Bcl-2 is a channel protein located on the mitochondrial membrane, which can inhibit the proapoptotic effect of Bax [44]. Activated p-AKT increased the expression of Bcl-2 and decreased the expression of Bax.…”
Section: Discussionmentioning
confidence: 99%
“…As is shown in Figure 8, the direct results of PI3K phosphorylation is the phosphorylation of AKT, which further affects the expression of Bcl-2 and Bax proteins. Bcl-2 and Bax are a group of proteins closely related to mitochondrial mediated apoptosis, among which the antiapoptotic protein Bcl-2 is a channel protein located on the mitochondrial membrane, which can inhibit the proapoptotic effect of Bax [44]. Activated p-AKT increased the expression of Bcl-2 and decreased the expression of Bax.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, cell death evasion is currently recognized as a hallmark of cancer. Several findings demonstrate pro-proliferative and anti-apoptotic signals cooperating in initial mammary epithelial cells transformation, where the anti-apoptotic Bcl-2 proteins are considered to play an important role [47]. Consistently, BC spread is faster when correlated to Bcl-2 overexpression, as well as genetic Bax ablation promotes mammary tumor development [48].…”
Section: Dysregulated Mechanisms Controlling Apoptosis and Cell Deathmentioning
confidence: 93%
“…In the context of cancer, genetic anomalies and unconventional microenvironments profit by endogenous pro-survival signaling to re-program and rewire metabolism to sustain survival, growth, and proliferation. It is now largely established that tumor is not simply a consequence of deregulated proliferation, but also of evasion from apoptosis, so the regulation of programmed cell death in cancer cells can be of critical importance in defining the overall growth or regression in response to treatments [45,47,152]. Besides being a major occurrence in the onset and progression of BC, malignant cells survival represents a crucial contributing factor also in clinical failure and chemoresistance development [153].…”
Section: Biological Responses To Nucleolipid Ru-based Nanoformulationmentioning
confidence: 99%
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“…The inactivated caspase-9 is related to the tumor survival of triple-negative BC, and Bcl-2 is a vital factor in the antiapoptosis defense mechanism of BC. [27][28][29] Similarly, LC3B and Atg5 are positive regulators of autophagy, while Beclin-1 is negative regulator of autophagy. Among them, LC3B is tied to BC immune infiltration, Atg5 is tied to BC tumor occurrence and metastasis, and Beclin-1 is tied to BC patient survival and chemotherapy sensitivity.…”
Section: Dovepressmentioning
confidence: 99%