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排序方式: 共有354条查询结果,搜索用时 15 毫秒
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Complex‐I Alteration and Enhanced Mitochondrial Fusion Are Associated With Prostate Cancer Progression
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Supriya Chakraborty Swatilekha Ghosh Bhaswati Banerjee Abhishek Santra Jyotsna Bhat Arghya Adhikary Subhrangsu Chatterjee Anup K. Misra Parimal C. Sen 《Apoptosis : an international journal on programmed cell death》2016,21(10):1106-1124
The efficacy of cancer chemotherapeutics is limited by side effects resulting from narrow therapeutic windows between the anticancer activity of a drug and its cytotoxicity. Thus identification of small molecules that can selectively target cancer cells has gained major interest. Cancer cells under stress utilize the Unfolded protein response (UPR) as an effective cell adaptation mechanism. The purpose of the UPR is to balance the ER folding environment and calcium homeostasis under stress. If ER stress is prolonged, tumor cells undergo apoptosis. In the present study we demonstrated an 3,3′-(Arylmethylene)-bis-1H-indole (AMBI) derivative 3,3′-[(4-Methoxyphenyl) methylene]-bis-(5-bromo-1H-indole), named as Mephebrindole (MPB) as an effective anti-cancer agent in breast cancer cells. MPB disrupted calcium homeostasis in MCF7 cells which triggered ER stress development. Detailed evaluations revealed that mephebrindole by activating p38MAPK also regulated GRP78 and eIF2α/ATF4 downstream to promote apoptosis. Studies extended to in vivo allograft mice models revalidated its anti-carcinogenic property thus highlighting the role of MPB as an improved chemotherapeutic option. 相似文献
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FBXL20 promotes breast cancer malignancy by inhibiting apoptosis through degradation of PUMA and BAX
Rajesh Kumar Manne Yashika Agrawal Sunil K. Malonia Shahid Banday Sarathkumar Edachery Asha Patel Avinash Kumar Praveenkumar Shetty Manas Kumar Santra 《The Journal of biological chemistry》2021,297(4)
Apoptosis is a programmed cell death that efficiently removes damaged cells to maintain tissue homeostasis. Defect in apoptotic machinery can lead to tumor development, progression, and resistance to chemotherapy. PUMA (p53 upregulated modulator of apoptosis) and BAX (BCL2-associated X protein) are among the most well-known inducers of apoptosis. It has been reported that expression levels of BAX and PUMA are controlled at the posttranslational level by phosphorylation. However, the posttranslational regulation of these proapoptotic proteins remains largely unexplored. In this study, using biochemical, molecular biology, flow cytometric, and immunohistochemistry techniques, we show that PUMA and BAX are the direct target of the F-box protein FBXL20, which restricts their cellular levels. FBXL20 directs the proteasomal degradation of PUMA and BAX in a protein kinase AKT1-dependent manner to promote cancer cell proliferation and tumor growth. Interestingly, inactivation of AKT1 results in activation of another protein kinase GSK3α/β, which facilitates the proteasomal degradation of FBXL20 by another F-box protein, FBXO31. Thus, a switch between two signaling kinases AKT1 and GSK3α/β modulates the functional activity of these proapoptotic regulators, thereby determining cell survival or death. RNAi-mediated ablation of FBXL20 results in increased levels of PUMA as well as BAX, which further enhances the sensitivity of cancer cells to chemotherapeutic drugs. We showed that high level expression of FBXL20 in cancer cells reduces therapeutic drug-induced apoptosis and promotes chemoresistance. Overall, this study highlights the importance of targeting FBXL20 in cancers in conjunction with chemotherapy and may represent a promising anticancer strategy to overcome chemoresistance. 相似文献
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Sampa Santra Ashwini K. Sood Swapan K. Ghosh 《Cancer immunology, immunotherapy : CII》1999,48(8):421-429
Active specific immunotherapy of neoplastic diseases is an elusive goal. Using a murine B lymphoma 2C3, we showed that vaccination
with the killed tumor cells effectively induces protective immunity and a cytotoxic T cell (CTL) response. Similar protection,
however, is rarely observed in mice bearing live tumor cells. These animals usually succumb to the progressively growing tumor.
In this study, we inquired whether the splenic CTL induced during tumor progression in mice differ from those evoked by the
killed tumor cells. Here we demonstrate that the CTL generated following vaccination are significantly different from those
induced in the tumor-bearing hosts. Adding to the complexity, the CTL from the early tumor bearers also differ significantly
from those induced at the late stages. These differences are based on their cytotoxic activity, MHC allele specificity, mitogen
responsiveness, cytokine secretion profile and T cell receptor Vβ gene expression. The results clearly indicate that passive
immunization with killed tumor is most effective, possibly because the CTL induced are not subject to the same regulatory
pressure as those induced during active tumor growth. This decreasing effectiveness of CTL could be due to greater variability
in antigenic stimulus, less involvement of innate immunity, changes in cytokine milieu and/or costimulatory factors.
Received: 5 February 1999 / Accepted: 22 June 1999 相似文献
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McCarthy BA Boyle E Wang XP Guzowski D Paul S Catera R Trott J Yan XJ Croce CM Damle R Yancopoulos S Messmer BT Lesser M Allen SL Rai KR Chiorazzi N 《Molecular medicine (Cambridge, Mass.)》2008,14(9-10):618-627
Since its discovery in follicular lymphoma cells at the breakpoint t(14;18), Bcl-2 has been studied extensively in many basic and clinical science settings. Bcl-2 can locate as an integral mitochondrial membrane component, where its primary role is to block apoptosis by maintaining membrane integrity. Here we show that Bcl-2 also can position on the outer cell surface membrane of B cells from patients with chronic lymphocytic leukemia (B-CLL) and certain other leukemias that do not classically possess the chromosomal breakpoint t(14;18). Although low levels of Bcl-2 can be detected on the surface membrane of apparently healthy leukemic and normal B cells, expression of Bcl-2 correlates best with spontaneous or induced apoptosis. Notably, upon induction of apoptosis, B-CLL cells were much more efficient in upregulating surface Bcl-2 than normal B cells. It is not clear if this surface membrane expression is a passive consequence of the apoptotic process or an active attempt by the B cell to abort cell death by stabilizing the plasma membrane. 相似文献
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Santanu Dasgupta Rex C. Yung William H. Westra David A. Rini Johann Brandes David Sidransky 《PloS one》2009,4(8)