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Molecular Cancer Research: MCR

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https://www.readbyqxmd.com/read/29784670/cancer-as-a-social-dysfunction-why-cancer-research-needs-new-thinking
#1
Kenneth J Pienta, Robert Axelrod
The incidence and mortality for many cancers continues to rise. As such, critical action is needed on many fronts to reshape how a society thinks, discusses, and fights cancer especially as the population grows and ages. Cancer can be described as a broken social contract which requires different conceptual frameworks such as game theory. To this end, it is our hope that this perspective will catalyze a discussion to rethink the way we approach, communicate, and fund cancer research - thinking of cancer as a broken social contract is only one example...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29784669/autophagy-cell-viability-and-chemo-resistance-are-regulated-by-mir-489-in-breast-cancer
#2
Hexin Chen, Mithil Soni, Yogin Patel, Eleni Markoutsa, Chunfa Jie, Shou Liu, Peisheng Xu
It is postulated that the complexity and heterogeneity in cancer may hinder most efforts that target a single pathway. Thus, discovery of novel therapeutic agents targeting multiple pathways, such as microRNAs (miRs), holds promise for future cancer therapy. One such miR, miR-489, is downregulated in majority of breast cancer cells and several drug-resistant breast cancer cell lines, but its role and underlying mechanism for tumor suppression and drug resistance needs further investigation. The current study identifies autophagy as a novel pathway targeted by miR-489 and reports Unc-51 like autophagy activating kinase 1 (ULK1) and lysosomal protein transmembrane 4 beta (LAPTM4B) to be direct targets of miR-489...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29784668/centrosome-linker-induced-tetraploid-segregation-errors-link-rhabdoid-phenotypes-and-lethal-colorectal-cancers
#3
Andrea Remo, Erminia Manfrin, Pietro Parcesepe, Alberto Ferrarini, Hye Seung Han, Mickys Ugnius, Carmelo Laudanna, Michele Simbolo, Donatella Malanga, Duarte Mendes Oliveira, Elisabetta Baritono, Tommaso Colangelo, Lina Sabatino, Jacopo Giuliani, Enrico Molinari, Marianna Garonzi, Luciano Xumerle, Massimo Delledonne, Guido Giordano, Claudio Ghimenton, Fortunato Lonardo, Fulvio D'angelo, Federica Grillo, Luca Mastracci, Giuseppe Viglietto, Michele Ceccarelli, Vittorio Colantuoni, Aldo Scarpa, Massimo Pancione
Centrosome anomalies contribute to tumorigenesis but it remains unclear how they are generated in lethal cancer phenotypes. Here, it is demonstrated that human microsatellite instable (MSI) and BRAF(V600E) mutant colorectal cancers with a lethal rhabdoid phenotype are characterized by inactivation of centrosomal functions. A splice site mutation that causes an unbalanced dosage of rootletin (CROCC), a centrosomal-linker component required for centrosome cohesion and separation at the chromosome 1p36.13 locus, resulted in abnormally shaped centrosomes in rhabdoid cells from human colon tissues...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29784667/pattern-specific-transcriptomics-identifies-asgr2-as-a-predictor-of-hematogenous-recurrence-of-gastric-cancer
#4
Haruyoshi Tanaka, Mitsuro Kanda, Takashi Miwa, Chie Tanaka, Daisuke Kobayashi, Shinichi Umeda, Masahiro Shibata, Masaya Suenaga, Norifumi Hattori, Masamichi Hayashi, Naoki Iwata, Suguru Yamada, Goro Nakayama, Michitaka Fujiwara, Yasuhiro Kodera
Hematogenous recurrence is a challenging clinical finding that often leads to fatalities of patients with gastric cancer. Therefore, the identification of specific biomarkers and potential therapeutic target molecules for hematogenous recurrence is required to improve the outcomes of these patients. Here, transcriptome and bioinformatics analyses were conducted to uncover candidate molecules differentially expressed in patients with hematogenous recurrence of gastric cancer. One potential candidate identified was asialoglycoprotein receptor 2 (ASGR2) and small interfering RNA (siRNA) experiments were conducted to determine the effect of manipulating ASGR2 expression has on cell phenotypes...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29784666/nomogram-integrating-genomics-with-clinicopathological-features-improves-prognosis-prediction-for-colorectal-cancer
#5
Yongfu Xiong, Wenxian You, Min Hou, Linglong Peng, He Zhou, Zhongxue Fu
The current tumor staging system is insufficient for predicting the outcomes of patients with colorectal cancer (CRC) because of its phenotypic and genomic heterogeneity. Integrating gene expression signatures with clinicopathological factors may yield a predictive accuracy exceeding that of the currently available system. Twenty-seven signatures that used gene expression data to predict CRC prognosis were identified and re-analyzed using bioinformatic methods. Next, clinically annotated CRC samples (n=1710) with the corresponding expression profiles, that predicted a patient's probability of cancer recurrence, were pooled to evaluate their prognostic values and establish a clinicopathologic-genomic nomogram...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29784665/srebf1-activity-is-regulated-by-an-ar-mtor-nuclear-axis-in-prostate-cancer
#6
Etienne Audet-Walsh, Mathieu Vernier, Tracey Yee, Chloe E Laflamme, Susan Li, Yonghong Chen, Vincent Giguere
Reprogramming of cellular metabolism is an important feature of prostate cancer (PCa), including altered lipid metabolism. Recently, it was observed that the nuclear fraction of mTOR is essential for the androgen-mediated metabolic reprogramming of PCa cells. Herein, it is demonstrated that the androgen receptor (AR) and mTOR bind to regulatory regions of sterol regulatory element binding transcription factor 1 (SREBF1) to control its expression, while dual activation of these signaling pathways also promotes SREBF1 cleavage and its translocation to the nucleus...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29769406/spindle-assembly-disruption-and-cancer-cell-apoptosis-with-a-cltc-binding-compound
#7
Michael J Bond, Marina Bleiler, Lauren E Harrison, Eric W Scocchera, Masako Nakanishi, Narendran G-Dayanandan, Santosh Keshipeddy, Daniel W Rosenberg, Dennis L Wright, Charles Giardina
AK3 compounds are mitotic-arrest agents that induce high levels of γH2AX during mitosis and apoptosis following release from arrest. We synthesized a potent AK3 derivative, AK306, that induced arrest and apoptosis of the HCT116 colon cancer cell line with an EC50 of ~50 nM. AK306 was active on a broad spectrum of cancer cell lines with total growth inhibition values ranging from ~25 nM to 25 µM. Using biotin and BODIPY-linked derivatives of AK306, binding to clathrin heavy chain (CLTC/CHC) was observed, a protein with roles in endocytosis and mitosis...
May 16, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29759990/epigenetic-targeting-of-adipocytes-inhibits-high-grade-serous-ovarian-cancer-cell-migration-and-invasion
#8
Jessica Tang, Nicholas Pulliam, Ali Ozes, Aaron Buechlein, Ning Ding, Doug Rusch, Harold Keer, Heather O'Hagan, M Sharon Stack, Kenneth P Nephew
Ovarian cancer (OC) cells frequently metastasize to the omentum and adipocytes play a significant role in ovarian tumor progression. Therapeutic interventions targeting aberrant DNA methylation in ovarian tumors have shown promise in the clinic but the effects of epigenetic therapy on the tumor microenvironment are understudied. Here, we examined the effect of adipocytes on OC cell behavior in culture and impact of targeting DNA methylation in adipocytes on OC metastasis. The presence of adipocytes increased OC cell migration and invasion and proximal and direct co-culture of adipocytes increased OC proliferation alone or after treatment with carboplatin...
May 14, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29759989/novel-regulation-of-integrin-trafficking-by-rab11-fip5-in-aggressive-prostate-cancer
#9
Lipsa Das, Jaime M C Gard, Rytis Prekeris, Raymond B Nagle, Colm Morrissey, Beatrice S Knudsen, Cindy K Miranti, Anne E Cress
The laminin-binding integrins, α3β1 and α6β1, are needed for tumor metastasis and their surface expression is regulated by endocytic recycling. β1 integrins share the Rab11 recycling machinery but the trafficking of α3β1 and α6β1 are distinct by an unknown mechanism. Using a mouse PDX tumor model containing human metastatic prostate cancer, Rab11 family interacting protein 5 (Rab11-FIP5) was identified as a lead candidate for α6β1 trafficking. Rab11-FIP5 and its membrane binding domain were required for α6β1 recycling, without affecting the other laminin-binding integrin (i...
May 14, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29759988/transient-telomerase-inhibition-with-imetelstat-impacts-dna-damage-signals-and-cell-cycle-kinetics
#10
Connor Ah Thompson, Alice Gu, Sunny Yang, Veena Mathew, Helen B Fleisig, Judy My Wong
Telomerase is the ribonucleoprotein reverse transcriptase that catalyzes the synthesis of telomeres at the ends of linear chromosomes and contributes to proper telomere-loop (T-loop) formation. Formation of the T-loop, an obligate step before cell division can proceed, requires the generation of a 3'-overhang on the G-rich strand of telomeric DNA via telomerase or C-strand specific nucleases. Here, it is discovered that telomerase activity is critical for efficient cell cycle progression using transient chemical inhibition by the telomerase inhibitor, imetelstat...
May 14, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29748382/satellite-rna-increases-dna-damage-and-accelerates-tumor-formation-in-mouse-models-of-pancreatic-cancer
#11
Takahiro Kishikawa, Motoyuki Otsuka, Tatsunori Suzuki, Takahiro Seimiya, Kazuma Sekiba, Rei Ishibashi, Eri Tanaka, Motoko Ohno, Mari Yamagami, Kazuhiko Koike
Highly repetitive tandem arrays such as satellite sequences in the centromeric and pericentromeric regions of chromosomes, which were previously considered to be silent, are actively transcribed in various biological processes, including cancers. In the pancreas, this aberrant expression occurs even in Kras-mutated pancreatic intraepithelial neoplasia (PanIN) tissues, which are precancerous lesions. To determine the biological role of satellite RNAs in carcinogenesis in vivo, we constructed mouse major satellite (MajSAT) RNA-expressing transgenic mice...
May 10, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29743296/yb-1-expression-and-phosphorylation-regulate-tumorigenicity-and-invasiveness-in-melanoma-by-influencing-emt
#12
Corinna Kosnopfel, Tobias Sinnberg, Birgit Sauer, Christian Busch, Heike Niessner, Anja Schmitt, Stephan Forchhammer, Cornelia Grimmel, Peter R Mertens, Stephan Hailfinger, Sandra E Dunn, Claus Garbe, Birgit Schittek
Cutaneous melanoma represents one of the most aggressive human tumor entities possessing a high tendency to metastasize. Cancer cells frequently exploit a highly conserved developmental program, the epithelial-to-mesenchymal transition (EMT), to gain migratory and invasive properties promoting their metastatic spread. Cytoplasmic localization of the oncogenic transcription and translation factor Y-box binding protein 1 (YB-1) is a powerful inducer of EMT in breast carcinoma cells. Interestingly, EMT-like processes have also been observed in cutaneous melanoma despite its neural crest origin...
May 9, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29739874/pten-regulates-non-homologous-end-joining-by-epigenetic-induction-of-nhej1-xlf
#13
Parker L Sulkowski, Susan E Scanlon, Sebastian Oeck, Peter M Glazer
DNA double-strand breaks (DSBs) are the most cytotoxic DNA lesions, and up to 90% of DSBs require repair by non-homologous end joining (NHEJ). Functional and genomic analyses of patient-derived melanomas revealed that PTEN loss is associated with NHEJ deficiency. In PTEN-null melanomas PTEN complementation rescued the NHEJ defect; conversely suppression of PTEN compromised NHEJ. Mechanistic studies revealed that PTEN promotes NHEJ through direct induction of expression of XRCC4-like factor (NHEJ1/XLF) which functions in DNA end bridging and ligation...
May 8, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29739873/p16-controls-p53-protein-expression-through-mir-dependent-destabilization-of-mdm2
#14
Huda Al-Khalaf, Abdelilah Aboussekhra
p16INK4A and p53 are two major tumor suppressor proteins, which are both up-regulated in response to various cellular stresses and during senescence and aging. p53 is a well characterized transcription factor, while p16INK4A a cyclin-dependent kinase inhibitor encoded by the CDKN2A gene, controls the expression of several genes through protein-protein interactions and also via microRNAs (miRs). This report demonstrates a p16INK4A-dependent positive regulation of p53 expression, at the protein level, in various human cells as well as in mouse embryonic fibroblasts (MEFs)...
May 8, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29724815/biomarker-assessment-of-hr-deficiency-tumor-brca1-2-mutations-and-ccne1-copy-number-in-ovarian-cancer-associations-with-clinical-outcome-following-platinum-monotherapy
#15
Euan A Stronach, James Paul, Kirsten M Timms, Elisha Hughes, Krystal Brown, Chris Neff, Michael Perry, Alexander Gutin, Mona El-Bahrawy, Jennifer H Steel, Xinxue Liu, Liz-Anne Lewsley, Nadeem Siddiqui, Hani Gabra, Jerry S Lanchbury, Robert Brown
The current study evaluated three biomarkers [homologous recombination deficiency (HRD), tumor BRCA1/2 (tBRCA) mutations, and CCNE1 copy number variation (CNV)] in ovarian tumors from patients enrolled on the SCOTROC4 clinical trial for associations with outcome following carboplatinum monotherapy. Ovarian tumors (n=250), with high-grade serous (HGSOC) subgroup analysis (n=179), were classified as HRD positive (HRD score ≥42 or tBRCA mutation) and as CCNE1 amplification positive (CCNE1 CNV score >2.4)...
May 3, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29724814/ahnak-loss-in-mice-promotes-type-ii-pneumocyte-hyperplasia-and-lung-tumor-development
#16
Jun Won Park, Il-Yong Kim, Ji Won Choi, Hee Jung Lim, Jae Hoon Shin, Yo Na Kim, Seo Hyun Lee, Yeri Son, Mira Sohn, Jong Kyu Woo, Joseph H Jeong, Cheolju Lee, Yun Soo Bae, Je Kyung Seong
AHNAK is known to be a tumor suppressor in breast cancer due to its ability to activate the TGFbeta signaling pathway. However, the role of AHNAK in lung tumor development and progression remains unknown. Here, the Ahnak gene was disrupted to determine its effect on lung tumorigenesis and the mechanism by which it triggers lung tumor development was investigated. First, AHNAK protein expression was determined to be decreased in human lung adenocarcinomas compared with matched non-neoplastic lung tissues. Then, Ahnak-/- mice were used to investigate the role of AHNAK in pulmonary tumorigenesis...
May 3, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29724813/egfrviii-stat5-signaling-enhances-glioblastoma-cell-migration-and-survival
#17
Alison Roos, Harshil D Dhruv, Sen Peng, Landon J Inge, Serdar Tuncali, Michael Pineda, Nghia Millard, Zachary Mayo, Jennifer M Eschbacher, Joseph C Loftus, Jeffrey A Winkles, Nhan L Tran
Glioblastoma multiforme (GBM) is the most common brain malignancies in adults. Most GBM patients succumb to the disease less than one year post-diagnosis due to the highly invasive nature of the tumor, which prevents complete surgical resection and gives rise to tumor recurrence. The invasive phenotype also confers radio- and chemo-resistant properties to the tumor cells; therefore, there is a critical need to develop new therapeutics that target drivers of GBM invasion. Amplification of EGFR is observed in over 50% of GBM tumors, of which half concurrently overexpress the variant EGFRvIII, and expression of both receptors confers a worse prognosis...
May 3, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29724812/usp11-enhances-tgf-946-induced-epithelial-mesenchymal-plasticity-and-human-breast-cancer-metastasis
#18
Daniel A Garcia, Christina Baek, M Valeria Estrada, Tiffani Tysl, Eric J Bennett, Jing Yang, John T Chang
Epithelial-mesenchymal transition (EMT) is a conserved cellular plasticity program that is reactivated in carcinoma cells and drives metastasis. While EMT is well studied its regulatory mechanisms remain unclear. Therefore, to identify novel regulators of EMT, a data mining approach was taken using published microarray data and a group of deubiquitinases (DUBs) were found to be upregulated in cells that have undergone EMT. Here, it is demonstrated that one DUB, ubiquitin specific peptidase 11 (USP11), enhances TGFβ-induced EMT and self-renewal in immortalized human mammary epithelial cells...
May 3, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29720480/targeting-usp22-suppresses-tumorigenicity-and-enhances-cisplatin-sensitivity-through-aldh1a3-downregulation-in-cancer-initiating-cells-from-lung-adenocarcinoma
#19
Xinwei Yun, Keqiang Zhang, Jinhui Wang, Rajendra P Pangeni, Lu Yang, Melissa Bonner, Jun Wu, Jami Wang, Isaac K Nardi, Ming Gao, Dan J Raz
Loss of monoubiquitination of histone H2B (H2Bub1) was found to be associated with poor-differentiation and enhanced malignancy of lung adenocarcinoma. This study, investigated the association and impact of the ubiquitin specific peptidase 22 (USP22), an H2Bub1 deubiquitinase, on stem cell-like characteristics and cisplatin resistance in cancer-initiating cells (CICs) from primary lung adenocarcinoma. CICs were isolated, enriched, and characterized from patient-derived cancer tissues using both in vitro tumorsphere formation and in vivo xenograft assays...
May 2, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29716964/nuclear-receptor-car-suppresses-gadd45b-p38-mapk-signaling-to-promote-phenobarbital-induced-proliferation-in-mouse-liver
#20
Takeshi Hori, Kosuke Saito, Rick Moore, Gordon P Flake, Masahiko Negishi
Phenobarbital (PB), a non-genotoxic hepatocarcinogen, induces hepatic proliferation and promotes development of hepatocellular carcinoma (HCC) in rodents. Nuclear receptor constitutive active/androstane receptor (NR1I3/CAR) regulates the induction and promotion activities of PB. Here, it is demonstrated that PB treatment results in dephosphorylation of a tumor suppressor p38 mitogen-activated protein kinase (MAPK) in the liver of C57BL/6 and C3H/HeNCrlBR mice. The molecular mechanism entails CAR binding and inhibition of the growth arrest and DNA-damage-inducible 45 beta (GADD45B)-MAPK kinase 6 (MKK6) scaffold to repress phosphorylation of p38 MAPK...
May 1, 2018: Molecular Cancer Research: MCR
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