BCL-2: Long and winding path from discovery to therapeutic target

Schenk, Robyn L; Strasser, Andreas; Dewson, Grant

doi:10.1016/j.bbrc.2016.10.100

Cited by 57 publications

(45 citation statements)

References 150 publications

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“…29 In the intrinsic pathway, cells triggered by intracellular stimuli through the Bcl-2 protein family activate caspase-9 and caspase-3. 30,31 In the present study, PPVI induced apoptosis in osteosarcoma cells by activating apoptosis pathways. Our data revealed that treatment of cells with PPVI increased expression of Bax, cleaved caspase-3, 8, and 9, and reduced Bcl-2 in glioma cells, confirming the occurrence of apoptosis.…”

Section: Discussionsupporting

confidence: 48%

<p>Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma</p>

Liu

Chai

et al. 2020

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Background: Polyphyllin VI (PPVI), a bioactive component derived from a traditional Chinese herb Paris polyphylla, exhibits potential antitumor activity against hepatocellular carcinoma, as well as breast and lung cancers. However, its effect on glioma remains unknown. Methods: Five glioma cell lines (U251, U343, LN229, U87 and HEB) and an animal model were employed in the study. Anti-proliferation effects of PPVI were first determined using CCK-8 cell proliferation and clone formation assays, then reactive oxygen species (ROS), cell cycle progression and apoptosis effects measured by flow cytometry. The effect of PPVI on protein expression was quantified by Western blot analysis. Results: Data showed that PPVI inhibited the proliferation of glioma cell lines by modulating the G2/M phase. Additionally, incubation of cells with PPVI promoted apoptosis, autophagy, increased accumulation of ROS and activated ROS-modulated JNK and p38 pathways. On the other hand, N-acetyl cysteine, a ROS inhibitor, attenuated PPVItriggered effects. Furthermore, JNK and p38 inhibitors ameliorated PPVI-triggered autophagy and apoptosis in glioma cells. In vivo assays showed that PPVI inhibited tumor growth of U87 cell line in nude mice. Conclusion: Overall, these data suggested that PPVI might be an effective therapeutic agent for glioma.

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Section: Discussionsupporting

confidence: 48%

<p>Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma</p>

Liu

Chai

et al. 2020

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“…SCC13 cells were treated with different concentrations of AL for 48 h, and then the expression levels of Bcl-2 and Bax and the relative proteins in MEK/NF-κB signaling pathway were measured. The present results suggested that Bcl-2, which plays an important role in apoptosis (20), was decreased in SCC13 cells after AL treatment (Fig. 4A and B).…”

Section: Avicularin Regulates the Expression Levels Of Apoptosis-relasupporting

confidence: 62%

Avicularin inhibits cell proliferation and induces cell apoptosis in cutaneous squamous cell carcinoma

et al. 2019

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Avicularin (AL), quercetin-3-α-L-arabinofur anoside, has various pharmacological properties such as anticancer and anti-infective effects. However, the potential molecular mechanism via which AL exerts its anticancer activity is not fully understood. Cutaneous squamous cell carcinoma (CSCC) is the second most common skin cancer, where metastasis has resulted in in effective clinical treatments. The aim of the present in vitro study was to investigate the anticancer effects and underlying mechanism of AL on human CSCC. The present results suggested that AL dose-dependently inhibited SCC13 cell viability and induced apoptosis. In addition, the present results suggested that AL induced apoptosis via repression of the mitogen-activated protein kinase kinase (MEK)/NF-κB signal pathway, thereby affecting the expression of apoptosis-related genes. Bax expression level was increased, while Bcl-2 expression level was decreased in SCC13 cells following AL treatment. In addition, the MEK/NF-κB signaling pathway-related genes p-MEK and phosphorylated-p65 were also decreased. The present results suggested that AL treatment increased the expression level of E-cadherin, but decreased the expression levels of N-cadherin, matrix metalloproteinase (MMP)-9 and vimentin in SCC13 cells. Collectively, the present results suggested that AL may have an anti-CSCC effect by inhibiting cell viability, inducing apoptosis and inhibiting epithelial-mesenchymal transition (EMT) of CSCC cells. The mechanism of these anti-CSCC effects was suggested to be via the regulation of apoptosis-related genes and EMT-related genes, and the inhibition of the MEK/NF-κB signaling pathway. Materials and methods Cell culture and treatment. DMEM (Gibco; Thermo Fisher Scientific, Inc) with 10% FBS (Gemini Bio-Products, Inc.), 10 U/ml penicillin-G and 10 mg/ml streptomycin (Gemini

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“…To further provide insight into the effect of E. faecalis on osteoblast apoptosis, the expression of members in the Bcl‐2 family was measured at 6 hr postinfection. The Bcl‐2 family has been considered as a key regulator of apoptosis through the intrinsic pathway in which the interaction between anti‐apoptotic Bcl‐2 and pro‐apoptotic Bax can determine the sensitivity of the cell to apoptotic stimuli (Schenk, Strasser, & Dewson, ). Bax is sequestered and inhibited by Bcl‐2 in healthy cells.…”

Section: Discussionmentioning

confidence: 99%