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Oncogene

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https://www.readbyqxmd.com/read/30413763/satb-family-chromatin-organizers-as-master-regulators-of-tumor-progression
#1
REVIEW
Rutika Naik, Sanjeev Galande
SATB (Special AT-rich binding protein) family proteins have emerged as key regulators that integrate higher-order chromatin organization with the regulation of gene expression. Studies over the past decade have elucidated the specific roles of SATB1 and SATB2, two closely related members of this family, in cancer progression. SATB family chromatin organizers play diverse and important roles in regulating the dynamic equilibrium of apoptosis, cell invasion, metastasis, proliferation, angiogenesis, and immune modulation...
November 9, 2018: Oncogene
https://www.readbyqxmd.com/read/30401983/acvr1c-smad2-signaling-promotes-invasion-and-growth-in-retinoblastoma
#2
Laura Asnaghi, David T White, Nolan Key, Joshua Choi, Alka Mahale, Hind Alkatan, Deepak P Edward, Sahar M Elkhamary, Saleh Al-Mesfer, Azza Maktabi, Christopher G Hurtado, Grace Y Lee, Angel M Carcaboso, Jeff S Mumm, Leen Abu Safieh, Charles G Eberhart
Retinoblastoma is the most common intraocular cancer in children. While the primary tumor can often be treated by local or systemic chemotherapy, metastatic dissemination is generally resistant to therapy and remains a leading cause of pediatric cancer death in much of the world. In order to identify new therapeutic targets in aggressive tumors, we sequenced RNA transcripts in five snap frozen retinoblastomas which invaded the optic nerve and five which did not. A three-fold increase was noted in mRNA levels of ACVR1C/ALK7, a type I receptor of the TGF-β family, in invasive retinoblastomas, while downregulation of DACT2 and LEFTY2, negative modulators of the ACVR1C signaling, was observed in most invasive tumors...
November 6, 2018: Oncogene
https://www.readbyqxmd.com/read/30401982/unbalanced-yap-sox9-circuit-drives-stemness-and-malignant-progression-in-esophageal-squamous-cell-carcinoma
#3
Lianghai Wang, Zhiyu Zhang, Xiaodan Yu, Xuan Huang, Zheng Liu, Yuhang Chai, Lei Yang, Qian Wang, Man Li, Jin Zhao, Jun Hou, Feng Li
Yes-associated protein (YAP) has been identified as a key regulator of tissue homeostasis. However, the precise role and regulatory mechanism of YAP in esophageal squamous cell carcinoma (ESCC) remains unclear. Here we report that the genetic or pharmacological inhibition of YAP repressed cancer stem cell (CSC)-like properties, including tumorsphere-forming potential, cell motility, and chemoresistance in vitro, and was sufficient to attenuate tumor growth and CSC marker expression in ESCC xenografts. Mechanistically, YAP transcriptionally activated its downstream target SOX9 via TEAD1-mediated binding...
November 6, 2018: Oncogene
https://www.readbyqxmd.com/read/30401981/taz-activation-by-hippo-pathway-dysregulation-induces-cytokine-gene-expression-and-promotes-mesothelial-cell-transformation
#4
Akihiro Matsushita, Tatsuhiro Sato, Satomi Mukai, Teruaki Fujishita, Emi Mishiro-Sato, Maho Okuda, Masahiro Aoki, Yoshinori Hasegawa, Yoshitaka Sekido
Malignant mesothelioma (MM) constitutes a very aggressive tumor that is caused by asbestos exposure after long latency. The NF2 tumor suppressor gene is mutated in 40-50% of MM; moreover, one of its downstream signaling cascades, the Hippo signaling pathway, is also frequently inactivated in MM cells. Although the YAP transcriptional coactivator, which is regulated by the Hippo pathway, can function as a pro-oncogenic protein, the role of TAZ, a paralog of YAP, in MM cells has not yet been clarified. Here, we show that TAZ is expressed and underphosphorylated (activated) in the majority of MM cells compared to immortalized mesothelial cells...
November 6, 2018: Oncogene
https://www.readbyqxmd.com/read/30397238/correction-cpg-island-hypermethylation-associated-silencing-of-non-coding-rnas-transcribed-from-ultraconserved-regions-in-human-cancer
#5
A Lujambio, A Portela, J Liz, S A Melo, S Rossi, R Spizzo, C M Croce, G A Calin, M Esteller
In the original article the authors have noted that the wrong image was used to illustrate the Uc.346 + Lu1-Lu2-Lu3 subpanel of Figure 5a. The correct image is now provided as Figure 1 in this article. This change does not affect the legend of the figure, the results, or conclusions reported in the manuscript. The authors apologize for the error, and regret any inconvenience this may have caused.
November 5, 2018: Oncogene
https://www.readbyqxmd.com/read/30390075/exosomal-wnt-induced-dedifferentiation-of-colorectal-cancer-cells-contributes-to-chemotherapy-resistance
#6
Y-B Hu, C Yan, L Mu, Y-L Mi, H Zhao, H Hu, X-L Li, D-D Tao, Y-Q Wu, J-P Gong, J-C Qin
Cancer stem cells (CSCs) are inherently resistant to chemotherapy, and CSCs in chemotherapy-failed recurrent tumors are enriched; however, the cellular origin of chemotherapy-induced CSC enrichment remains unclear. Communication with stromal fibroblasts may induce cancer cell dedifferentiation into CSCs through secreted factors. We recently demonstrated that fibroblast-derived exosomes promote chemoresistance in colorectal cancer (CRC). Here, we report that fibroblasts confer CRC chemoresistance via exosome-induced reprogramming (dedifferentiation) of bulk CRC cells to phenotypic and functional CSCs...
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30390074/tissue-necrosis-and-its-role-in-cancer-progression
#7
Adi Karsch-Bluman, Ariel Feiglin, Eliran Arbib, Tal Stern, Hila Shoval, Ouri Schwob, Michael Berger, Ofra Benny
Great efforts have been made in revealing the mechanisms governing cancer resistance and recurrence. The in-situ effects of cell death, caused by hypoxia and metabolic stress, were largely studied in association with inflammation. However, in this work, we focused on the direct effects of necrosis on cancer promotion and on the tumor microenvironment. The conditions leading to cell necrosis, upon nutrient and oxygen deprivation, were recapitulated in-vitro and were used to generate samples for computational proteomic analysis...
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30390073/p53-dependent-autophagic-degradation-of-tet2-modulates-cancer-therapeutic-resistance
#8
Jixiang Zhang, Peng Tan, Lei Guo, Jing Gong, Jingjing Ma, Jia Li, Minjung Lee, Shaohai Fang, Ji Jing, Gavin Johnson, Deqiang Sun, Wen-Ming Cao, Roderick Dashwood, Leng Han, Yubin Zhou, Wei-Guo Dong, Yun Huang
Tumor cells with p53 inactivation frequently exhibit chemotherapy resistance, which poses a long-standing challenge to cancer treatment. Here we unveiled a previously unrecognized role of TET2 in mediating p53-loss induced chemotherapy resistance in colon cancer. Deletion of TET2 in p53-null colon cancer cells enhanced DNA damage and restored chemotherapy sensitivity. By taking a two-pronged approach that combined pharmacological inhibition with genetic depletion, we discovered that p53 destabilized TET2 at the protein level by promoting its autophagic degradation...
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30390072/oncogenic-microrna-411-promotes-lung-carcinogenesis-by-directly-targeting-suppressor-genes-spry4-and-txnip
#9
Caiyan Zhang, Huimin Wang, Xiaomin Liu, Yanping Hu, Lei Ding, Xing Zhang, Qiangling Sun, Yanli Li
Lung cancer is one of the most common malignant diseases globally, composed of non-small cell lung cancer (NSCLC, 85%) and small cell lung cancer (SCLC, 15%). MicroRNAs (miRNAs) are single-stranded noncoding RNAs having important roles in lung cancer development. miR-411-5p/3p were reported to be increased significantly in human NSCLC tissues and cell lines. Moreover, miR-411-5p/3p overexpression could accelerate cell proliferation and migration, and impede cell apoptosis in NSCLC cell lines. Mechanically, SPRY4 is confirmed a direct target of miR-411-5p/3p...
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30390071/overexpression-mediated-activation-of-met-in-the-golgi-promotes-her3-erbb3-phosphorylation
#10
Nicole Michael Frazier, Toni Brand, John D Gordan, Jennifer Grandis, Natalia Jura
Ligand-dependent oligomerization of receptor tyrosine kinases (RTKs) results in their activation through highly specific conformational changes in the extracellular and intracellular receptor domains. These conformational changes are unique for each RTK subfamily, limiting cross-activation between unrelated RTKs. The proto-oncogene MET receptor tyrosine kinase overcomes these structural constraints and phosphorylates unrelated RTKs in numerous cancer cell lines. The molecular basis for these interactions is unknown...
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30390070/correction-aspm-promotes-prostate-cancer-stemness-and-progression-by-augmenting-wnt-dvl-3-%C3%AE-catenin-signaling
#11
Vincent C Pai, Chung-Chi Hsu, Tze-Sian Chan, Wen-Ying Liao, Chih-Pin Chuu, Wei-Yu Chen, Chi-Rong Li, Ching-Yu Lin, Shu-Pin Huang, Li-Tzong Chen, Kelvin K Tsai
In the published version of this paper the author Shu-Pin Huang's surname was incorrectly given as Hwang instead of Huang. This has now been corrected in the HTML and PDF versions of the paper.
November 2, 2018: Oncogene
https://www.readbyqxmd.com/read/30385854/bioinformatics-based-analysis-reveals-elevated-mfsd12-as-a-key-promoter-of-cell-proliferation-and-a-potential-therapeutic-target-in-melanoma
#12
Chuan-Yuan Wei, Meng-Xuan Zhu, Nan-Hang Lu, Rui Peng, Xuan Yang, Peng-Fei Zhang, Lu Wang, Jian-Ying Gu
Although recent therapeutic advances based on our understanding of molecular phenomena have prolonged the survival of melanoma patients, the prognosis of melanoma remains dismal and further understanding of the underlying mechanism of melanoma progression is needed. In this study, differential expression analyses revealed that many genes, including AKT1 and CDK2, play important roles in melanoma. Functional analyses of differentially expressed genes (DEGs), obtained from the GEO (Gene Expression Omnibus) database, indicated that high proliferative and metastatic abilities are the main characteristics of melanoma and that the PI3K and MAPK pathways play essential roles in melanoma progression...
November 1, 2018: Oncogene
https://www.readbyqxmd.com/read/30382189/the-role-of-gli-sox2-signaling-axis-for-gemcitabine-resistance-in-pancreatic-cancer
#13
Yanfei Jia, Dongsheng Gu, Jun Wan, Beiqin Yu, Xiaoli Zhang, E Gabriela Chiorean, Yunshan Wang, Jingwu Xie
Pancreatic cancer, mostly pancreatic ductal adenocarcinomas (PDAC), is one of the most lethal cancers, with a dismal median survival around 8 months. PDAC is notoriously resistant to chemotherapy. Thus far, numerous attempts using novel targeted therapies and immunotherapies yielded limited clinical benefits for pancreatic cancer patients. It is hoped that delineating the molecular mechanisms underlying drug resistance in pancreatic cancer may provide novel therapeutic options. Using acquired gemcitabine resistant pancreatic cell lines, we revealed an important role of the GLI-SOX2 signaling axis for regulation of gemcitabine sensitivity in vitro and in animal models...
October 31, 2018: Oncogene
https://www.readbyqxmd.com/read/30375491/correction-overexpression-of-mir-489-derails-mammary-hierarchy-structure-and-inhibits-her2-neu-induced-tumorigenesis
#14
Y Patel, M Soni, A Awgulewitsch, M J Kern, S Liu, N Shah, U P Singh, H Chen
In the published version of this paper the author A. Awgulewitsch's surname was incorrectly given as Awagulerwitsch instead of Awgulewitsch. This has now been corrected in the HTML version of the paper, the PDF was correct at the time of publication.
October 30, 2018: Oncogene
https://www.readbyqxmd.com/read/30368528/igfbp2-promotes-vasculogenic-mimicry-formation-via-regulating-cd144-and-mmp2-expression-in-glioma
#15
Y Liu, F Li, Y T Yang, X D Xu, J S Chen, T L Chen, H J Chen, Y B Zhu, J Y Lin, Y Li, X M Xie, X L Sun, Y Q Ke
Vasculogenic mimicry (VM) refers to the fluid-conducting channels formed by aggressive tumor cells rather than endothelial cells (EC) with elevated expression of genes associated with vascularization. VM has been considered as one of the reasons that glioblastoma becomes resistant to anti-VEGF therapy. However, the molecular basis underlying VM formation remains unclear. Here we report that the insulin-like growth factor-binding protein 2 (IGFBP2) acts as a potent factor to enhance VM formation in glioma. Evidence showed that elevated IGFBP2 expression was positively related with VM formation in patients with glioma...
October 27, 2018: Oncogene
https://www.readbyqxmd.com/read/30367150/bclaf1-promotes-angiogenesis-by-regulating-hif-1%C3%AE-transcription-in-hepatocellular-carcinoma
#16
Ying Wen, Xueqiong Zhou, Meiting Lu, Meiling He, Ye Tian, Lixia Liu, Mengnan Wang, Wenchong Tan, Yaotang Deng, Xushan Yang, Matthias P Mayer, Fei Zou, Xuemei Chen
The development of hepatocellular carcinomas (HCC) depends on their local microenvironment and the induction of neovascularization is a decisive step in tumor progression, since the growth of solid tumors is limited by nutrient and oxygen supply. Hypoxia is the critical factor that induces transcription of the hypoxia inducible factor-1α (HIF-1α) encoding gene HIF1A and HIF-1α protein accumulation to promote angiogenesis. However, the basis for the transcriptional regulation of HIF1A expression in HCC is still unclear...
October 26, 2018: Oncogene
https://www.readbyqxmd.com/read/30367149/forcing-atgl-expression-in-hepatocarcinoma-cells-imposes-glycolytic-rewiring-through-ppar-%C3%AE-p300-mediated-acetylation-of-p53
#17
Luca Di Leo, Rolando Vegliante, Fabio Ciccarone, Illari Salvatori, Manuel Scimeca, Elena Bonanno, Andrea Sagnotta, Gian Luca Grazi, Katia Aquilano, Maria Rosa Ciriolo
Metabolic reprogramming is a typical feature of cancer cells aimed at sustaining high-energetic demand and proliferation rate. Here, we report clear-cut evidence for decreased expression of the adipose triglyceride lipase (ATGL), the first and rate-limiting enzyme of triglyceride hydrolysis, in both human and mouse-induced hepatocellular carcinoma (HCC). We identified metabolic rewiring as major outcome of ATGL overexpression in HCC-derived cell lines. Indeed, ATGL slackened both glucose uptake/utilization and cell proliferation in parallel with increased oxidative metabolism of fatty acids and enhanced mitochondria capacity...
October 26, 2018: Oncogene
https://www.readbyqxmd.com/read/30361686/adipose-stromal-cell-targeting-suppresses-prostate-cancer-epithelial-mesenchymal-transition-and-chemoresistance
#18
Fei Su, Songyeon Ahn, Achinto Saha, John DiGiovanni, Mikhail G Kolonin
Fat tissue, overgrowing in obesity, promotes the progression of various carcinomas. Clinical and animal model studies indicate that adipose stromal cells (ASC), the progenitors of adipocytes, are recruited by tumors and promote tumor growth as tumor stromal cells. Here, we investigated the role of ASC in cancer chemoresistance and invasiveness, the attributes of tumor aggressiveness. By using human cell co-culture models, we demonstrate that ASC induce epithelial-mesenchymal transition (EMT) in prostate cancer cells...
October 25, 2018: Oncogene
https://www.readbyqxmd.com/read/30361685/dual-inhibition-of-pi3k-signaling-and-histone-deacetylation-halts-proliferation-and-induces-lethality-in-mantle-cell-lymphoma
#19
Hui Guo, Dongfeng Zeng, Hui Zhang, Taylor Bell, Jun Yao, Yang Liu, Shengjian Huang, Carrie J Li, Elizabeth Lorence, Shouhao Zhou, Tiejun Gong, Changying Jiang, Makhdum Ahmed, Yixin Yao, Krystle J Nomie, Liang Zhang, Michael Wang
The dysregulation of PI3K signaling has been implicated as an underlying mechanism associated with resistance to Bruton's tyrosine kinase inhibition by ibrutinib in both chronic lymphocytic leukemia and mantle cell lymphoma (MCL). Ibrutinib resistance has become a major unmet clinical need, and the development of therapeutics to overcome ibrutinib resistance will greatly improve the poor outcomes of ibrutinib-exposed MCL patients. CUDC-907 inhibits both PI3K and HDAC functionality to exert synergistic or additive effects...
October 25, 2018: Oncogene
https://www.readbyqxmd.com/read/30356139/targeting-surface-nucleolin-induces-autophagy-dependent-cell-death-in-pancreatic-cancer-via-ampk-activation
#20
Cheng Xu, Yunfei Wang, Qiu Tu, Zhiye Zhang, Mengrou Chen, James Mwangi, Yaxiong Li, Yang Jin, Xudong Zhao, Ren Lai
Pancreatic cancer remains one of the deadliest human cancers despite current advances in conventional therapeutics including surgery and adjuvant therapies. Here, we showed that LZ1, a peptide derived from a snake venom cathelicidin, significantly inhibited growth of pancreatic cancer cells by inducing autophagy-dependent cell death both in vitro and in vivo. The LZ1-induced cell death was blocked by pharmacological or genetic inhibition of autophagy. In orthotopic model of pancreatic cancer, systemic administration of LZ1 (1-4 mg/kg) exhibited remarkable antitumor efficacy, significantly prolonged mice survival, and showed negligible adverse effects by comparison with gemcitabine (20 mg/kg)...
October 24, 2018: Oncogene
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