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Inhibition of autophagy by autophagic inhibitors enhances apoptosis induced by bortezomib in non-small cell lung cancer cells.

作者信息

Wu Guodong, Li Haifeng, Ji Zhiyong, Jiang Xiaoming, Lei Yu, Sun Mingli

机构信息

Department of Cardiovascular, Regenerative Medicine and Tissue Engineering, First Affiliated Hospital of Jilin University, Changchun, 130021, Jilin, China,

出版信息

Biotechnol Lett. 2014 Jun;36(6):1171-8. doi: 10.1007/s10529-014-1470-0. Epub 2014 Feb 22.

DOI:10.1007/s10529-014-1470-0
PMID:24563301
Abstract

Bortezomib is a novel proteasome inhibitor that has promising antitumor activity against various cancer cells. We have assessed its antitumor activity in non-small cell lung cancer (NSCLC) A549 and H157 cells in vitro where it inhibited cell growth and induced apoptosis, which was associated with cytochrome c release and caspase-3 activation. Bortezomib upregulated autophagic-related proteins, the Atg12-Atg5 complex and LC3-II, which indicated autophagy had occurred. The combination of bortezomib with autophagic inhibitor 3-methyladenine or chloroquine significantly enhanced suppression of cell growth and apoptosis induced by bortezomib in A549 and H157 cells. Our study indicated that inhibition of both proteasome and autophagy has great potential for NSCLC treatment.

摘要

相似文献

1
Inhibition of autophagy by autophagic inhibitors enhances apoptosis induced by bortezomib in non-small cell lung cancer cells.
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2
Romidepsin induces cell cycle arrest, apoptosis, histone hyperacetylation and reduces matrix metalloproteinases 2 and 9 expression in bortezomib sensitized non-small cell lung cancer cells.罗米地辛诱导细胞周期停滞、细胞凋亡，使组蛋白乙酰化，并降低硼替佐米增敏的非小细胞肺癌细胞中基质金属蛋白酶 2 和 9 的表达。
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Bortezomib enhances cancer cell death by blocking the autophagic flux through stimulating ERK phosphorylation.硼替佐米通过刺激细胞外信号调节激酶（ERK）磷酸化来阻断自噬流，从而增强癌细胞死亡。
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The proteasome inhibitor PS-341 (bortezomib) up-regulates DR5 expression leading to induction of apoptosis and enhancement of TRAIL-induced apoptosis despite up-regulation of c-FLIP and survivin expression in human NSCLC cells.蛋白酶体抑制剂PS-341（硼替佐米）上调DR5表达，尽管人非小细胞肺癌细胞中c-FLIP和生存素表达上调，但仍可诱导细胞凋亡并增强TRAIL诱导的细胞凋亡。
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SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.SAHA可诱导肝癌细胞凋亡，并与蛋白酶体抑制剂硼替佐米协同作用。
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Proteasome inhibitor interacts synergistically with autophagy inhibitor to suppress proliferation and induce apoptosis in hepatocellular carcinoma.蛋白酶体抑制剂与自噬抑制剂协同作用，抑制肝癌细胞增殖并诱导其凋亡。
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Effect of Oleanolic Acid on Apoptosis and Autophagy of SMMC-7721 Hepatoma Cells.
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Oncol Lett. 2016 Jul;12(1):63-68. doi: 10.3892/ol.2016.4606. Epub 2016 May 18.
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Autophagy is associated with cucurbitacin D-induced apoptosis in human T cell leukemia cells.自噬与葫芦素D诱导人T细胞白血病细胞凋亡有关。
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Inhibition of autophagy induced by quercetin at a late stage enhances cytotoxic effects on glioma cells.槲皮素在晚期对自噬的抑制增强了对胶质瘤细胞的细胞毒性作用。
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