IndraLab

Statements


Bortezomib decreases the amount of BCL2. 23 / 36
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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 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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"Similarly, Yang and colleagues found that bortezomib also decreases the levels of Bcl-2 in the H520 and H460 NSCLC cell lines, by 60% and 50%, respectively [71] ."

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"When the apoptotic signaling was tested, we found that bortezomib induced the cleavage of caspase 9, caspase 3 and PARP while reducing the expression of anti-apoptotic protein Bcl-2 in SW872 cells."

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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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"These EVs blocked the significant reduction of Bcl-2 expression caused by bortezomib and reduced cleaved caspase-9, caspase-3, and PARP either in the absence or presence of bortezomib."

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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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"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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"In addition to NF–κB inhibition, we found that sequential use of etoposide and bortezomib strongly suppressed the expression of bcl-2."

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"In our experimental study we also found that bcl-2 was strongly induced by etoposide, whereas bortezomib only slightly inhibited the bcl-2 expression."

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

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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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"RT-qPCR assay confirmed that the combination of BOR and VEM could enhance the mRNA expression of STK3 (MST2) (Additional file 1: Fig. S6G), and WB assay confirmed that the combination of BOR and VEM could enhance the expression of BAX and MST2, and reduce the expression of BCL-2, TAZ and YAP1 (Fig. 7F), which was consistent with the results in vitro."

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

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