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Molecular & Cellular Oncology

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https://www.readbyqxmd.com/read/30525101/expanding-the-chemotherapeutic-potential-of-an-established-nucleoside-analog-with-selective-targeting-of-telomerase
#1
Tawna L Whited, Derek J Taylor
The identification of telomerase-mediated telomeric misincorporation of 5-fluoro-2'-deoxyuridine (5-FdU) uncovered a unique approach to telomeric-based therapeutics. Additionally, identification of such a mechanism supports the utility of telomere maintenance mechanisms in guiding therapeutic decisions. Presented here is a unique perspective of 5-FdU and its clinical implications as a telomeric-based therapeutic.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525100/trim16-controls-turnover-of-protein-aggregates-by-modulating-nrf2-ubiquitin-system-and-autophagy-implication-for-tumorigenesis
#2
Kautilya Kumar Jena, Srinivasa Prasad Kolapalli, Subhash Mehto, Swati Chauhan, Santosh Chauhan
Protein misfolding and protein aggregation are linked to several diseases commonly called as proteinopathies, which include cancer. Understanding the mechanisms of proteostasis could provide newer strategies to combat proteinopathies. We have recently demonstrated a new mechanism where we found that TRIM16 (tripartite motif-containing protein 16) utilizing NRF2-p62 axis and autophagy streamlines the safe disposal of misfolded proteins to maintain protein homeostasis.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525099/ykt6-mediates-autophagosome-vacuole-fusion
#3
Levent Bas, Daniel Papinski, Claudine Kraft
Studying the mechanism of autophagosome-vacuole fusion has proven difficult in live yeast cells. Developing a novel in vitro fusion assay, we identified Ykt6 as the missing R-SNARE (Soluble N -ethylmaleimide sensitive factor attachment protein receptor) in this process and pinpoint the place of action of all four SNAREs involved. Parallel studies have confirmed our findings in other organisms.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525098/-esr1-fusions-drive-endocrine-therapy-resistance-and-metastasis-in-breast-cancer
#4
Jonathan T Lei, Xuxu Gou, Matthew J Ellis
Estrogen receptor alpha gene ( ESR1 ) fusion transcripts have been identified in breast cancer but their role in breast cancer is not completely understood. Here, we report a causal role for ESR1 fusions in driving both endocrine therapy resistance and metastasis, and describe a therapeutic strategy to target ESR1 fusion-induced growth.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525097/cisplatin-resistance-coupled-to-enhanced-sensitivity-to-metabolic-interventions
#5
Maria Castedo, Florine Obrist, Guido Kroemer
Specific metabolic alterations have recently been observed in cisplatin-resistant cancers. As a result, cisplatin resistance can be overcome by co-administration of pyridoxine, and cisplatin-resistant cancer cells become exquisitely sensitive to killing by inhibitors of poly(ADP-ribose) polymerase, starvation, and antimetabolites targeting nucleotide biosynthesis.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525096/stitching-up-broken-dna-ends-by-fanca
#6
Anna Palovcak, Wenjun Liu, Fenghua Yuan, Yanbin Zhang
RAD52 rejoins resected broken DNA ends by mediating single-strand annealing. Our recent work elucidates that FANCA, a Fanconi anemia protein, also directly repairs double-strand breaks (DSBs) by catalyzing annealing of single-stranded DNA. FANCA and RAD52 likely play complementary roles to each other to prevent deleterious consequences of DSBs. Abbreviations: DSBs: DNA double-strand breaks; ICL: interstrand crosslink; ssDNA: single-stranded DNA; HR: homologous recombination; SSA: single-strand annealing; MMEJ: microhomology-mediated end joining; NHEJ: non-homologous end joining; GFP: green fluorescence protein...
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525095/controlling-the-mitochondrial-antisense-role-of-the-suv3-pnpase-complex-and-its-co-factor-grsf1-in-mitochondrial-rna-surveillance
#7
Zbigniew Pietras, Magdalena A Wojcik, Lukasz S Borowski, Maciej Szewczyk, Tomasz M Kulinski, Dominik Cysewski, Piotr P Stepien, Andrzej Dziembowski, Roman J Szczesny
Transcription of the human mitochondrial genome produces a vast amount of non-coding antisense RNAs. These RNA species can form G-quadraplexes (G4), which affect their decay. We found that the mitochondrial degradosome, a complex of RNA helicase SUPV3L1 (best known as SUV3) and the ribonuclease PNPT1 (also known as PNPase), together with G4-melting protein GRSF1, is a key player in restricting antisense mtRNAs.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525094/oncogenic-regulatory-circuits-driven-by-19q13-rs11672691-underlies-prostate-cancer-aggressiveness
#8
Ji-Han Xia, Gong-Hong Wei
The 19q13 allele rs11672691 has been reproducibly found in association with aggressive form of prostate cancer, yet the underlying mechanism remains totally unknown. We have recently uncovered a mechanism by which rs11672691 influenced a novel oncogenic regulatory circuit, including HOXA2, PCAT19 and CEACAM21 , thereby contributing to prostate cancer aggressiveness.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525093/timed-degradation-of-mcl-1-controls-mitotic-cell-death
#9
Paul R Clarke, Lindsey A Allan, Agnieszka Skowyra
Mitotic arrest can result in cell death through the process of apoptosis. We have shown by live-cell imaging that the ubiquitin-proteasome dependent proteolysis of the apoptotic regulator Mcl-1 under the control of the anaphase-promoting complex or cyclosome (APC/C) provides a timing mechanism that distinguishes prolonged mitotic arrest from normal mitosis.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525092/wobble-uridine-trna-modification-a-new-vulnerability-of-refractory-melanoma
#10
Francesca Rapino, Pierre Close
The enzymes catalysing the modification of the wobble uridine (U34 ) of tRNAs (U34 -enzymes) play an important role in tumor development. We have recently demonstrated that the U34 -enzymes are crucial in the survival of glycolytic melanoma cultures through a codon-specific regulation of HIF1α mRNA translation. Moreover, depletion of U34 -enzymes resensitizes resistant melanoma to targeted therapy. These results indicate that targeting U34 -enzymes represents a new therapeutic opportunity for melanoma patients...
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525091/breaking-bad-family-ties-pan-erbb-blockers-inhibit-kras-driven-lung-tumorigenesis
#11
Herwig P Moll, Emilio Casanova
Oncogenic K-RAS mutations were believed to lock the molecular switch in the ON state, independent of upstream activation. However, we demonstrate in preclinical models that activity of mutated K-RAS depends on upstream signaling events involving EGF receptor family members. This finding reveals a potential therapeutic vulnerability using pan-ERBB inhibitors to fight K-RAS mutated lung tumors.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525090/on-your-marks-get-set-d1a-the-race-to-protect-stalled-replication-forks
#12
Shabana Begum, Amalia Goula, Rachel Bayley, Martin R Higgs
We recently identified that methylation of lysine 4 of histone H3 (H3K4) by SETD1A (SET domain containing 1A) maintains genome stability by protecting newly-replicated DNA from degradation. Mechanistically, SETD1A-dependent histone methylation regulates nucleosome mobilisation by FANCD2 (FA complementation group D2), a crucial step in maintaining genome integrity with important implications in chemo-sensitivity.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525089/functional-characterization-of-the-p53-mutome
#13
Eran Kotler, Eran Segal, Moshe Oren
Phenotypic characterization of mutations in the tumor protein p53 ( TP53 ) gene has so far focused on a handful of relatively frequent "hotspot" mutations, accounting for only ~ 30% of cases. We expanded the scope and quantitatively measured the impact of thousands of distinct TP53 mutations in vitro and in vivo , providing insights into the connections between structure, function, evolutionary conservation and clinical impact.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525088/with-great-power-comes-great-vulnerability
#14
Rodrigo Leite de Oliveira, Liqin Wang, Rene Bernards
The clinical responses to targeted drugs are often transient and do not always translate into meaningful overall survival due to the development of resistance. We discuss here that the greater power of drug resistant cells can be associated with significant newly-acquired vulnerabilities that can be exploited therapeutically.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525087/micrornas-novel-regulators-of-the-tgf-%C3%AE-pathway-in-pancreatic-ductal-adenocarcinoma
#15
Silvia Ottaviani, Leandro Castellano
We identified that transforming growth factor-β (TGF-β) induces long non-coding RNA (lncRNA) MIR100HG along with its host microRNAs (miRNAs) miR-100 and miR-125b, to regulate its response in pancreatic ductal adenocarcinoma (PDAC). Importantly let-7a, despite originating from MIR100HG, remains unchanged because post-transcriptionally repressed by lin-28 homolog B (LIN28B). A novel method for global miRNA-target discovery identified that miR-100/125b regulates crucial PDAC pathways.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525086/the-role-of-plk1-in-cancer-exhibiting-chromosomal-instability
#16
Klaus Strebhardt, Monika Raab, Mourad Sanhaji
Adenomatous polyposis coli (APC) mutations cause aneuploidy and are responsible for familial adenomatous polyposis characterized by chromosomal instability. PLK1 contributes to sustain an intact spindle assembly checkpoint ensuring genomic stability. In our work using independent ApcMin/+ mouse models we revealed that PLK1 functions as tumor suppressor in APC-mutated colorectal cancers.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30525085/carcinoma-cells-reprogram-a-wound-healing-switch-to-promote-metastasis
#17
Gopinath M Sundaram, Prabha Sampath
Wound healing is a dynamic event where barrier disruption is transient and miR-198/FSTL1 molecular switch orchestrate wound re-epithelialization. However, epithelial carcinomas maintain a prolonged wound-healing phase to promote malignant transformation. Delineating the molecular mechanism we demonstrate, how epidermal growth factor (EGF) hijacks the wound-healing switch to promote metastasis of carcinoma.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30263950/dna-repair-synthesis-and-histone-deposition-partner-during-homologous-recombination
#18
Amira Elbakry, Szilvia Juhász, Arthur Mathes, Markus Löbrich
Chromatin remodeling is critical for the regulation of the DNA damage response. We highlight findings from our recent study showing that the deposition of the histone variant H3.3 by the alpha-thalassemia mental retardation X-linked protein (ATRX) and the death domain associated protein (DAXX) chromatin remodeling complex regulates DNA repair synthesis during homologous recombination.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30263949/local-unwinding-of-double-strand-dna-ends-by-the-mrx-complex-promotes-exo1-processing-activity
#19
Elisa Gobbini, Jacopo Vertemara, Maria Pia Longhese
Homologous recombination is initiated by nucleolytic degradation (resection) of DNA double-strand breaks (DSBs), which involves different nucleases including the Mre11-Rad50-Xrs2 (MRX) complex and the Exonuclease 1 (Exo1). The characterization of a novel mutation in Mre11 causing accelerated DSB resection has allowed to show that MRX facilitates DNA end processing by Exo1 through local unwinding of double-stranded DNA ends.
2018: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/30263948/cdk6-at-the-interface-of-rb-and-p53
#20
Sofie Nebenfuehr, Florian Bellutti, Veronika Sexl
In cancer the activity of cyclin-dependent kinase 4-(CDK4) and cyclin-dependent kinase 6 (CDK6)-cyclin complexes are frequently altered with enhanced CDK6 expression found in hematopoietic malignancies. Our latest findings show a so far unknown role of Cdk6 during oncogene-induced stress and transformation. Therein Cdk6 antagonizes p53 responses and subsequently shapes the critical decision between survival and apoptosis in pre-leukemic cells.
2018: Molecular & Cellular Oncology
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