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Molecular & Cellular Oncology

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https://read.qxmd.com/read/30788425/etiological-involvement-of-cftr-in-apparently-unrelated-human-diseases
#1
Lorenzo Galluzzi, Guido Kroemer
No abstract text is available yet for this article.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788424/patient-derived-xenografts-a-promising-resource-for-preclinical-cancer-research
#2
Christina Karamboulas, Laurie Ailles
Patient-derived xenograft tumors retain molecular and histopathological features of the originating tumor and are useful preclinical tools for drug discovery and assessment. We recently reported that 'rapid' engraftment of head and neck squamous cell carcinoma samples is highly prognostic and correlates with deregulation of the G1/S checkpoint. Tumors with genetic alterations in cyclinD1 ( CCND1) and/or cyclin-dependent kinase inhibitor 2A ( CDKN2A) are more likely to respond to abemaciclib.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788423/phosphatidic-acid-a-lipid-regulator-of-the-hippo-pathway
#3
Han Han, Rebecca Vargas, Gayoung Seo, Wenqi Wang
The Hippo pathway, a signaling pathway highly conserved across species, plays a crucial role in organ size control and cancer suppression. Our recent study shows that phosphatidic acid can regulate the Hippo pathway through a physical lipid-protein interaction, providing additional insights into the Hippo-related tissue homeostasis and cancer development.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788422/oncogenic-%C3%AE-catenin-mutations-evade-ph-regulated-degradation
#4
Bree K Grillo-Hill, Katharine A White
β-catenin has roles in cell-cell adhesion and Wnt signaling. We recently showed that β-catenin protein abundance is decreased at higher intracellular pH (pHi), mediated by pH-sensitive interaction with the beta-transducin repeat containing E3 ubiquitin protein ligase (β-TrCP). Increased pHi facilitates β-TrCP binding and degradation of β-catenin. β-catenin mutations that abrogate the pH-sensitive interaction induce significant tumors not seen with other β-catenin stabilizing mutants.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788421/lncrnas-join-hands-together-to-regulate-neuroblastoma-progression
#5
Tanmoy Mondal, Chandrasekhar Kanduri
Trait associated single nucleotide polymorphisms often overlap with noncoding transcripts but their contribution to disease phenotype is poorly investigated. Our study on neuroblastoma risk associated 6p22.3 locus derived long noncoding RNAs (lncRNAs) demonstrates that functional co-operation between sense-antisense CASC15 and NBAT1 lncRNAs control neuroblastoma progression via regulating SOX9-CHD7-USP36 regulatory axis.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788420/novel-mechanism-of-resistance-to-targeted-therapies-in-lung-cancer
#6
Walter Wang, David P Carbone, Rajeswara Rao Arasada
We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor ( EGFR ) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β-catenin) stability and increased survival of drug persister cells (DPCs). Furthermore, combined treatment of an EGFR TKI with a β-catenin inhibitor demonstrated improved therapeutic outcomes in xenograft models.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788419/author-s-view-epithelial-plasticity-metabolically-reprograms-normal-cells-towards-a-neoplastic-prone-state
#7
Hailun Wang, Phuoc T Tran
We have uncovered that epithelial plasticity programs metabolically reprogram epithelial lung cells by increasing expression of genes (e.g., glutamine-fructose-6-phosphate transaminase 2 - GFPT2 and UDP-N-acetylglucosamine pyrophosphorylase 1 - UAP1 ) critical for the hexosamine biosynthetic pathway (HBP) and elevating global protein O-GlcNAcylation - a specific type of glycosylation. We found that increased O-GlcNAcylation could suppress oncogene-induced senescence tumor suppressor pathways that ultimately led to accelerated KrasG12D -driven lung tumorigenesis...
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788418/the-role-of-r-loops-in-transcription-associated-dna-double-strand-break-repair
#8
Reona Kato, Kiyoshi Miyagawa, Takaaki Yasuhara
The roles of RNA in the DNA damage response are emerging. We highlight findings from our recent study demonstrating the mechanism for transcription-associated homologous recombination repair (TA-HRR) of DNA double-strand breaks and the critical role of R-loops in TA-HRR.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788417/cancer-stem-cells-here-there-and-everywhere
#9
Sophie C Lodestijn, Kristiaan J Lenos, Daniël M Miedema, Maarten F Bijlsma, Louis Vermeulen
By using marker-free lineage tracing in combination with quantitative analysis, we recently revealed cancer stem cell functionality in established human colon cancer is not intrinsically defined, but fully spatiotemporally regulated.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788416/mtorc1-driven-accumulation-of-the-oncometabolite-fumarate-as-a-potential-critical-step-in-renal-cancer-progression
#10
Luca Drusian, Alessandra Boletta
Modeling renal cancer in the mouse has been challenging. We recently showed that upregulation of mechanistic target of rapamycin complex 1 (mTORC1) in a restricted segment of the renal tubule leads to downregulation of the tricarboxylic acid (TCA) cycle enzyme fumarate hydratase, to accumulation of the oncometabolite fumarate, and gradual transformation from benign cysts into cystadenomas and papillary carcinomas.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788415/bap1-suppresses-tumor-development-by-inducing-ferroptosis-upon-slc7a11-repression
#11
Yilei Zhang, Li Zhuang, Boyi Gan
The tumor suppressor BRCA1-associated protein 1 (BAP1) is a deubiquitinase that removes histone 2A ubiquitination. How BAP1 suppresses tumor development remains elusive. Our recent study identified the cystine transporter solute carrier family 7 member 11 (SLC7A11) as a critical BAP1 target, and showed that BAP1 promotes ferroptosis (a non-apoptotic cell death) through repressing SLC7A11 expression, resulting in tumor suppression.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788414/senescence-controls-prostatic-neoplasia-driven-by-pten-loss
#12
Maxime Parisotto, Elise Grelet, Rana El Bizri, Daniel Metzger
We report that Pten (phosphatase and tensin homologue) ablation in prostatic epithelial cells of adult mice promotes cell proliferation to generate prostatic intraepithelial neoplasia. Moreover, our results demonstrate that proliferating Pten-deficient cells undergo replication stress and exhibit a DNA damage response, leading to cell senescence, as seen in oncogene-induced senescence.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30788413/increasing-the-accuracy-of-glioblastoma-subtypes-factoring-in-the-tumor-s-cell-of-origin
#13
Sven Nelander
The transcriptional classification of glioblastoma has proven to be a complex issue. In the absence of strong correlations between underlying genomic lesions and transcriptional subtype, there is a need to systematically understand the origins of the glioblastoma subtypes. A recent integrated analysis of data from both mouse models and patient-derived cells supports that the glioblastoma's cell of origin is important in shaping transcriptional diversity and tumor cell malignancy.
2019: Molecular & Cellular Oncology
https://read.qxmd.com/read/30525101/expanding-the-chemotherapeutic-potential-of-an-established-nucleoside-analog-with-selective-targeting-of-telomerase
#14
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://read.qxmd.com/read/30525100/trim16-controls-turnover-of-protein-aggregates-by-modulating-nrf2-ubiquitin-system-and-autophagy-implication-for-tumorigenesis
#15
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://read.qxmd.com/read/30525099/ykt6-mediates-autophagosome-vacuole-fusion
#16
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://read.qxmd.com/read/30525098/-esr1-fusions-drive-endocrine-therapy-resistance-and-metastasis-in-breast-cancer
#17
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://read.qxmd.com/read/30525097/cisplatin-resistance-coupled-to-enhanced-sensitivity-to-metabolic-interventions
#18
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://read.qxmd.com/read/30525096/stitching-up-broken-dna-ends-by-fanca
#19
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://read.qxmd.com/read/30525095/controlling-the-mitochondrial-antisense-role-of-the-suv3-pnpase-complex-and-its-co-factor-grsf1-in-mitochondrial-rna-surveillance
#20
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
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