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Richa Bajpai et al.
Nature communications, 11(1), 1228-1228 (2020-03-08)
The BCL-2 antagonist venetoclax is highly effective in multiple myeloma (MM) patients exhibiting the 11;14 translocation, the mechanistic basis of which is unknown. In evaluating cellular energetics and metabolism of t(11;14) and non-t(11;14) MM, we determine that venetoclax-sensitive myeloma has
Lara Grande et al.
The Journal of biological chemistry, 287(32), 26495-26505 (2012-06-22)
Testicular germ cell tumors (TGCTs) are highly responsive to and curable by cisplatin-based chemotherapy even in advanced stages. We have studied the molecular mechanisms involved in the induction of apoptosis in response to cisplatin, and found that proapoptotic Noxa is
Xinying Li et al.
Oncology letters, 17(2), 1851-1858 (2019-01-25)
Esophageal squamous cell carcinoma (ESCC) is a dominant histological subtype of esophageal cancer with notably high incidence and mortality rates. Pemetrexed is a clinical antifolate therapeutic agent with anticancer properties. The present study aimed to understand whether pemetrexed is able
Benigno C Valdez et al.
Leukemia & lymphoma, 58(11), 2705-2716 (2017-04-11)
The combination of gemcitabine (Gem), busulfan (Bu), and melphalan (Mel) is a promising regimen for autologous stem-cell transplantation (SCT) for lymphomas. To further improve the efficacy of [Gem + Bu + Mel], we added poly(ADP-ribose) polymerase (PARP) inhibitor olaparib (Ola). We hypothesized that Ola
Yiru Zhang et al.
Cancer research, 80(1), 30-43 (2019-11-07)
The receptor kinase c-MET has emerged as a target for glioblastoma therapy. However, treatment resistance emerges inevitably. Here, we performed global metabolite screening with metabolite set enrichment coupled with transcriptome and gene set enrichment analysis and proteomic screening, and identified
Clara Lucía León-Annicchiarico et al.
The FEBS journal, 282(18), 3647-3658 (2015-07-15)
Altered metabolism is a hallmark of cancer that opens new therapeutic possibilities. 2-deoxyglucose (2-DG) is a non-metabolizable glucose analog tested in clinical trials and is frequently used in experimental settings to mimic glucose starvation. However, in the present study, conducted
Feng Yun Yang et al.
Bioengineered, 13(1), 1377-1387 (2022-01-04)
Dexmedetomidine (DEX) has been reported to attenuate the ischemia and reperfusion (I/R) induced cardiomyocyte apoptosis. However, mechanisms underlying these protective effect remain to be fully elucidated. Cardiomyocyte apoptosis is associated with ischemic heart disease. Here we investigated the role of
Wenjuan Zhang et al.
Cell proliferation, 52(2), e12536-e12536 (2018-10-21)
The present study aimed to reveal expression status of the neddylation enzymes in HNSCC and to elucidate the anticancer efficacy and the underlying mechanisms of inhibiting neddylation pathway. The expression levels of neddylation enzymes were estimated by Western blotting in
Jieun Yun et al.
Journal of cellular physiology, 230(12), 3115-3127 (2015-06-03)
p53 and Notch-1 play important roles in breast cancer biology. Notch-1 inhibits p53 activity in cervical and breast cancer cells. Conversely, p53 inhibits Notch activity in T-cells but stimulates it in human keratinocytes. Notch co-activator MAML1 binds p53 and functions
Danrui Cui et al.
Cell reports, 30(2), 497-509 (2020-01-16)
The tumor suppressor p53 plays a critical role in integrating a wide variety of stress responses. Therefore, p53 levels are precisely regulated by multiple ubiquitin ligases. In this study, we report that FBXW7, a substrate recognition component of the SKP1-CUL1-F-box
Qing Yu et al.
Neoplasia (New York, N.Y.), 22(4), 179-191 (2020-03-08)
Cullin-RING E3 ligase (CRL) is the largest family of E3 ubiquitin ligase, responsible for ubiquitylation of ∼20% of cellular proteins. CRL plays an important role in many biological processes, particularly in cancers due to abnormal activation. CRL activation requires neddylation
Cameron S Fraser et al.
Nature communications, 13(1), 5789-5789 (2022-10-03)
Immunoglobulin light chain (AL) amyloidosis is an incurable hematologic disorder typically characterized by the production of amyloidogenic light chains by clonal plasma cells. These light chains misfold and aggregate in healthy tissues as amyloid fibrils, leading to life-threatening multi-organ dysfunction.
Tsung-Ming Yang et al.
American journal of respiratory cell and molecular biology, 41(1), 14-23 (2008-12-23)
Combinatorial therapies using the proteasome inhibitor, bortezomib, have been found to induce synergistic apoptosis in cancer cells grown as monolayers; however, three-dimensional spheroid culture may be a better model for the multicellular resistance found in solid tumors, such as lung
Ryan Soderquist et al.
Apoptosis : an international journal on programmed cell death, 19(1), 201-209 (2013-09-28)
S1 is a putative BH3 mimetic proposed to inhibit BCL2 and MCL1 based on cell-free assays. However, we previously demonstrated that it failed to inhibit BCL2 or induce apoptosis in chronic lymphocytic leukemia (CLL) cells, which are dependent on BCL2
Joanna Zawacka-Pankau et al.
The Journal of biological chemistry, 286(48), 41600-41615 (2011-08-25)
Unique sensitivity of tumor cells to the inhibition of glycolysis is a good target for anticancer therapy. Here, we demonstrate that the pharmacologically activated tumor suppressor p53 mediates the inhibition of glycolytic enzymes in cancer cells in vitro and in
Shaheen Kabir et al.
eLife, 8 (2019-07-12)
Overexpression of anti-apoptotic proteins MCL1 and Bcl-xL are frequently observed in many cancers. Inhibitors targeting MCL1 are in clinical development, however numerous cancer models are intrinsically resistant to this approach. To discover mechanisms underlying resistance to MCL1 inhibition, we performed
Mateus Milani et al.
Cell death discovery, 5, 117-117 (2019-07-26)
Maintenance of mitochondrial integrity is critical for normal cellular homoeostasis. Most cells respond to stress stimuli and undergo apoptosis by perturbing mitochondrial structure and function to release proteins, such as cytochrome c, which are essential for the execution of the
Yanchun Wang et al.
Cancer biology & therapy, 16(3), 420-429 (2015-03-18)
Recent studies indicate that post-translational protein neddylation is required for the maintenance of cell viability in several lymphoma cell lines, while inhibition of the neddylation pathway with an NEDD8-activating enzyme (NAE) inhibitor MLN4924 induces apoptosis in lymphoma cells. However, the
Min Ji Seo et al.
Cell death & disease, 10(3), 187-187 (2019-02-24)
Gambogic acid (GA), a xanthonoid extracted from the resin of the tree, Garcinia hanburyi, was recently shown to exert anticancer activity in multiple studies, but the underlying action mechanism remains unclear. Here, we show that GA induces cancer cell death
Shuxi Qiao et al.
Biochemical pharmacology, 83(9), 1229-1240 (2012-02-11)
Pharmacological induction of oxidative and proteotoxic stress has recently emerged as a promising strategy for chemotherapeutic intervention targeting cancer cells. Guided by a differential phenotypic drug screen for novel lead compounds that selectively induce melanoma cell apoptosis without compromising viability
Jing Cui et al.
Cancer cell international, 15(1), 4-4 (2015-02-17)
BIX-01294, an euchromatic histone-lysine N-methyltransferase 2 (EHMT2) inhibitor, has been reported to induce apoptosis in human neuroblastoma cells and inhibit the proliferation of bladder cancer cells. However, the definite mechanism of the apoptosis mediated by BIX-01294 in bladder cancer cells
David J Mallick et al.
Cancers, 12(8) (2020-08-23)
Anti-apoptotic BCL2 proteins are important targets for cancer therapy as cancers depend on their activity for survival. Direct inhibitors of MCL1 have entered clinical trials, although their efficacy may be limited by toxicity. An alternative approach may be to induce
Angela L Davis et al.
The Journal of biological chemistry, 290(3), 1623-1638 (2014-12-06)
Pharmacological induction of proteotoxic stress is rapidly emerging as a promising strategy for cancer cell-directed chemotherapeutic intervention. Here, we describe the identification of a novel drug-like heat shock response inducer for the therapeutic induction of proteotoxic stress targeting malignant human
J-S Diallo et al.
British journal of cancer, 99(10), 1613-1622 (2008-10-23)
Effective treatments for androgen-independent prostate cancer (AIPCa) are lacking. To address this, emerging therapeutics such as proteasome inhibitors are currently undergoing clinical trials. Inositol hexakisphosphate (IP6) is an orally non-toxic phytochemical that exhibits antitumour activity against several types of cancer
Marie-Christine Albert et al.
Cell death & disease, 11(9), 740-740 (2020-09-12)
The BH3-only protein NOXA is a regulator of mitochondrial apoptosis by specifically antagonizing the anti-apoptotic protein MCL-1. Here we show that the E3 ubiquitin ligase CHIP controls NOXA stability after DNA damage. Our findings reveal that CHIP and MCL-1 are
Kerstin Brinkmann et al.
Cell reports, 3(3), 881-891 (2013-03-19)
The BH3-only protein NOXA represents one of the critical mediators of DNA-damage-induced cell death. In particular, its involvement in cellular responses to cancer chemotherapy is increasingly evident. Here, we identify a strategy of cancer cells to escape genotoxic chemotherapy by
Danrui Cui et al.
Cell death & disease, 11(11), 976-976 (2020-11-14)
DEP-domain containing mTOR-interacting protein (DEPTOR), a natural mTOR inhibitor, has essential roles in several processes, including cell growth, metabolism, apoptosis, and immunity. DEPTOR expression has been shown to be diversely controlled at transcriptional levels in cell- and context-specific manners. However
L-H Meng et al.
Oncogene, 26(33), 4806-4816 (2007-02-14)
Aminoflavone (AF, NSC 686,288) is beginning clinical trials. It induces replication-mediated histone H2AX phosphorylation, DNA-protein crosslinks and activates p53. Here, we studied p21(CIP1/WAF1) and Mdm2 responses to AF. Although p53 stabilization and phosphorylation at serine 15 increased with dose and
Xiao-Lan Li et al.
Oncology reports, 45(5) (2021-04-14)
p53‑reactivation and induction of massive apoptosis‑1, APR‑017 methylated (PRIMA‑1met; APR246) targets mutant p53 to restore its wild‑type structure and function. It was previously demonstrated that PRIMA‑1met effectively inhibited the growth of colorectal cancer (CRC) cells in a p53‑independent manner, and distinctly
Barbara Schroeder et al.
Cell death & disease, 12(11), 977-977 (2021-10-23)
Inhibitors of the lipogenic enzyme fatty acid synthase (FASN) have attracted much attention in the last decade as potential targeted cancer therapies. However, little is known about the molecular determinants of cancer cell sensitivity to FASN inhibitors (FASNis), which is
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