IndraLab

Statements


Bortezomib decreases the amount of BCL2. 30 / 30
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"From table 1 of full text: bortezomib suppressed constitutive NF-kappaB activation via I-kappaB stabilisation in three ATL cell lines (TaY, MT-2 and MT-4). An oligonucleotide DNA microarray analysis of TaY cells revealed upregulation of genes encoding heat shock proteins (HSPA1A, STIP1, HSPA1B, and HSPCA), genes related to protein folding (CDC37 and ANAPC5), Fas-associated factor 1(FAF1) and an oxidative stress-related gene, heme oxygenase-1(HMOX-1), known to be a target gene of hypoxia-inducible gene-1 alpha (HIF-1 alpha)."

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"Western blot analysis demonstrated that bortezomib treatment significantly decreased the expression levels of Bcl-2 (XREF_FIG) and LC3-II (XREF_FIG), and increased the expression levels of p62, cleaved PARP and cleaved caspase-3 (XREF_FIG) in shBeclin-1 NB4 cells compared with in shCTRL cells."

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"MSC-exo inhibits the reduction of Bcl-2 expression caused by bortezomib and reduces the cleavage of caspase-9, caspase-3, and PARP."

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"In this model, in cells expressing p50 NFkappaB, the Bcl-2 promoter would be occupied predominantly by p50/50 homodimers, which would not regulate Bcl-2 transcription, and thus Bcl-2 expression would not be suppressed by the bortezomib induced nuclear IkappaBalpha."

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"Bortezomib induced apoptosis was further demonstrated by increased levels of cleaved caspase-3, cleaved PARP and Bax, and decreased expression levels of Bcl-2 (XREF_FIG and XREF_SUPPLEMENTARY)."

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"Bortezomib slightly decreased Bcl-2 expression, but increased the expression and cleavage of Mcl-1 (XREF_FIG), which was abolished by the caspase inhibitors, Z-VAD, Z-IETD and Z-LEHD (XREF_FIG)."

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"PS-341 downregulated the expression of Bcl-2 and Bcl-xl in protein levels at an early time of treatment."

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"Conversely, in cells that do not express p50 NFkappaB, the Bcl-2 promoter might be occupied by other NFkappaB dimers, which regulate Bcl-2 transcription, and thus in these cells, Bcl-2 transcription would be inhibited by bortezomib."

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"Furthermore, the 26S proteasome inhibitor bortezomib can downregulate Bcl-2 expression."

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"Bortezomib targets pathways relevant to tumor progression and therapy resistance and can directly modulate expression of cyclins, p27kip1, p53, nuclear factor-kB, Bcl-2, and Bax."

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"Bortezomib treatment in the knockdown cells increased the levels of cleaved caspase-3 and cleaved PARP, and decreased the expression levels of Bcl-2, indicating that autophagy inhibition in combination with proteasome suppression resulted in increased apoptosis."

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"Bortezomib treatment decreased BCL2 and MCL1 levels in a dose dependent manner in both D1-GFP- and GFP expressing clones, but this effect was stronger in cyclin D1 expressing cells."

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"Bortezomib has been shown to reduce Bcl-2 levels and induce apoptosis in the H526 SCLC cell line [XREF_BIBR]."

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"The results showed that 11.55 nM HHT or 1.12 nM Bortezomib significantly increased cleavage activation of caspase 9 and caspase 3, inhibited anti-apoptotic protein Bcl-2 expression and upregulated pro apoptotic protein Bax."

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"PS-341 not only inhibited nuclear localization of NF-kappaB but also activated the caspase cascade, increased p21 and Bax levels, and decreased Bcl-2 levels."

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"Bortezomib arrested the cell cycles of three cell lines at the G2/M stage, decreased BCL2 mRNA expression, but did not affect MDR1 mRNA levels."

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"Preclinical studies demonstrated that bortezomib reduced Bcl-2 levels and induced apoptosis in small cell lung cancer cell lines."

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"The addition of bortezomib to docetaxel maintains p27 induction and decreases levels of Bcl-2, enhancing docetaxel cytotoxicity."