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Oncogenesis

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https://www.readbyqxmd.com/read/27892920/foxk1-interaction-with-fhl2-promotes-proliferation-invasion-and-metastasis-in-colorectal-cancer
#1
M Wu, J Wang, W Tang, X Zhan, Y Li, Y Peng, X Huang, Y Bai, J Zhao, A Li, C Chen, Y Chen, H Peng, Y Ren, G Li, S Liu, J Wang
The transcriptional factor Forkhead box k1 (FOXK1) is a member of the FOX family. The abnormal expression of FOXK1 may have an important role in tumour development. Our previous studies showed that four-and-a-half LIM protein 2 (FHL2) is a critical inducer of the epithelial-to-mesenchymal transition (EMT) and invasion. However, the molecular mechanism by which FOXK1 synergizes with FHL2 tumour proliferation, EMT and metastasis is not well defined. We evaluated that messenger RNA (mRNA) and protein expression levels by quantitative RT-PCR, western blot, immunofluorescence and immunohistochemistry (IHC) assays...
November 28, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27869785/classic-il-6r-signalling-is-dispensable-for-intestinal-epithelial-proliferation-and-repair
#2
K Aden, A Breuer, A Rehman, H Geese, F Tran, J Sommer, G H Waetzig, T M Reinheimer, S Schreiber, S Rose-John, J Scheller, P Rosenstiel
Inflammatory bowel disease is characterized by disturbed cytokine signalling in the mucosa. Inhibition of the proinflammatory interleukin (IL)-6 pathway is a promising new therapeutic strategy, but safety concerns arise as IL-6 signalling also contributes to epithelial repair of the intestinal mucosa. To which extent IL-6 classic or trans-signalling contributes to intestinal repair remains elusive. We tested the influence of IL-6 classic signalling on intestinal repair and proliferation. Whereas IL-6 induced STAT3 phosphorylation in the colonic cancer cell lines, primary non-malignant intestinal organoids did not respond to IL-6 classic signalling...
November 21, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27841855/notch3-inhibits-epithelial-mesenchymal-transition-by-activating-kibra-mediated-hippo-yap-signaling-in-breast-cancer-epithelial-cells
#3
X Zhang, X Liu, J Luo, W Xiao, X Ye, M Chen, Y Li, G-J Zhang
Invasion, metastasis and chemoresistance are leading causes of death in breast cancer patients. A vital change of epithelial cells, epithelial-mesenchymal transition (EMT), is involved in these processes. Unfortunately, the molecular mechanisms controlling EMT remain to be elucidated. Our previous studies have shown that ectopic N3ICD expression inhibits EMT in MDA-MB-231, a triple-negative breast cancer (TNBC) epithelial cell line. To decipher the mechanism, we performed in-depth studies. Specifically, we found that overexpressing N3ICD transcriptionally upregulated the expression of Kibra, an upstream member of the Hippo pathway...
November 14, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27819668/sall4-promotes-gastric-cancer-progression-through-activating-cd44-expression
#4
X Yuan, X Zhang, W Zhang, W Liang, P Zhang, H Shi, B Zhang, M Shao, Y Yan, H Qian, W Xu
The stem cell factor SALL4 (Sal-like protein 4) plays important roles in the development and progression of cancer. SALL4 is critically involved in tumour growth, metastasis and therapy resistance. However, the underlying mechanisms responsible for the oncogenic roles of SALL4 have not been well characterized. In this study, we demonstrated that SALL4 knockdown by short hairpin RNA greatly inhibited the proliferation, migration and invasion of gastric cancer cells. We further confirmed the inhibitory effects of SALL4 knockdown on gastric cancer cells by using a tetracycline-inducible system...
November 7, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27797363/constitutively-activated-pi3k-accelerates-tumor-initiation-and-modifies-histopathology-of-breast-cancer
#5
M R Sheen, J D Marotti, M J Allegrezza, M Rutkowski, J R Conejo-Garcia, S Fiering
The gene encoding phosphatidylinositol 3-kinase catalytic subunit α-isoform (PIK3CA, p110α) is frequently activated by mutation in human cancers. Based on detection in some breast cancer precursors, PIK3CA mutations have been proposed to have a role in tumor initiation. To investigate this hypothesis, we generated a novel mouse model with a Cre-recombinase regulated allele of p110α (myristoylated-p110α, myr-p110α) along with p53(fl/fl) deletion and Kras(G12D) also regulated by Cre-recombinase. After instillation of adenovirus-expressing Cre-recombinase into mammary ducts, we found that myr-p110α accelerated breast tumor initiation in a copy number-dependent manner...
October 31, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27775701/gpr133-adgrd1-an-adhesion-g-protein-coupled-receptor-is-necessary-for-glioblastoma-growth
#6
N S Bayin, J D Frenster, J R Kane, J Rubenstein, A S Modrek, R Baitalmal, I Dolgalev, K Rudzenski, L Scarabottolo, D Crespi, L Redaelli, M Snuderl, J G Golfinos, W Doyle, D Pacione, E C Parker, A S Chi, A Heguy, D J MacNeil, N Shohdy, D Zagzag, D G Placantonakis
Glioblastoma (GBM) is a deadly primary brain malignancy with extensive intratumoral hypoxia. Hypoxic regions of GBM contain stem-like cells and are associated with tumor growth and angiogenesis. The molecular mechanisms that regulate tumor growth in hypoxic conditions are incompletely understood. Here, we use primary human tumor biospecimens and cultures to identify GPR133 (ADGRD1), an orphan member of the adhesion family of G-protein-coupled receptors, as a critical regulator of the response to hypoxia and tumor growth in GBM...
October 24, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27775700/axl-egfr-receptor-tyrosine-kinase-hetero-interaction-provides-egfr-with-access-to-pro-invasive-signalling-in-cancer-cells
#7
M Vouri, D R Croucher, S P Kennedy, Q An, G J Pilkington, S Hafizi
Acquired resistance to conventional and targeted therapies is becoming a major hindrance in cancer management. It is increasingly clear that cancer cells are able to evolve and rewire canonical signalling pathways to their advantage, thus evading cell death and promoting cell invasion. The Axl receptor tyrosine kinase (RTK) has been shown to modulate acquired resistance to EGFR-targeted therapies in both breast and lung cancers. Glioblastoma multiforme (GBM) is a highly infiltrative and invasive form of brain tumour with little response to therapy...
October 24, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27775699/susd2-expression-in-high-grade-serous-ovarian-cancer-correlates-with-increased-patient-survival-and-defective-mesothelial-clearance
#8
J N Sheets, M Iwanicki, J F Liu, B E Howitt, M S Hirsch, J A A Gubbels, R Drapkin, K A Egland
The cause of death among the majority of epithelial ovarian cancer (EOC) patients involves passive dissemination of cancer cells within the peritoneal cavity and subsequent implantation of cancer spheroids into adjacent organs. Thus, it is important to identify the factors that mediate EOC metastasis and implantation, including clearance of the mesothelium. Sushi domain containing 2 (SUSD2) encodes a type I transmembrane protein containing several functional domains inherent to adhesion molecules. Immunohistochemical analysis determined the presence of SUSD2 in several subtypes of EOC, with the strongest staining observed in high-grade serous ovarian carcinomas (HGSOCs)...
October 24, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27694836/the-zn-finger-domain-of-mdmx-suppresses-cancer-progression-by-promoting-genome-stability-in-p53-mutant-cells
#9
Z Matijasevic, A Krzywicka-Racka, G Sluder, J Gallant, S N Jones
The MDMX (MDM4) oncogene is amplified or overexpressed in a significant percentage of human tumors. MDMX is thought to function as an oncoprotein by binding p53 tumor suppressor protein to inhibit p53-mediated transcription, and by complexing with MDM2 oncoprotein to promote MDM2-mediated degradation of p53. However, down-regulation or loss of functional MDMX has also been observed in a variety of human tumors that are mutated for p53, often correlating with more aggressive cancers and a worse patient prognosis...
October 3, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27694835/the-interplay-between-hpip-and-casein-kinase-1%C3%AE-promotes-renal-cell-carcinoma-growth-and-metastasis-via-activation-of-mtor-pathway
#10
H Mai, X Xu, G Mei, T Hong, J Huang, T Wang, Z Yan, Y Li, Y Liang, L Li, S Jin, W You, Y Ma, L Chen, Q Ye
Hematopoietic pre-B cell leukemia transcription factor (PBX)-interacting protein (HPIP) was shown to be crucial during the development and progression of a variety of tumors. However, the role of HPIP in renal cell carcinoma (RCC) is unknown. Here we report that HPIP is upregulated in most RCC patients, positively correlates with tumor size, high Fuhrman grade and preoperative metastasis, and predicts poor clinical outcomes. Mechanistically, we identified casein kinase 1α (CK1α), a critical regulator of tumorigenesis and metastasis, as a novel HPIP-interacting protein...
October 3, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27694834/duox1-silencing-in-lung-cancer-promotes-emt-cancer-stem-cell-characteristics-and-invasive-properties
#11
A C Little, D Sham, M Hristova, K Danyal, D E Heppner, R A Bauer, L M Sipsey, A Habibovic, A van der Vliet
Dual oxidase 1 (DUOX1) is an oxidant-generating enzyme within the airway epithelium that participates in innate airway host defense and epithelial homeostasis. Recent studies indicate that DUOX1 is suppressed in lung cancers by epigenetic silencing, although the importance of DUOX1 silencing in lung cancer development or progression is unknown. Here we show that loss of DUOX1 expression in a panel of lung cancer cell lines is strongly associated with loss of the epithelial marker E-cadherin. Moreover, RNAi-mediated DUOX1 silencing in lung epithelial cells and the cancer cell line NCI-H292 was found to result in loss of epithelial characteristics/molecular features (altered morphology, reduced barrier function and loss of E-cadherin) and increased mesenchymal features (increased migration, anchorage-independent growth and gain of vimentin/collagen), suggesting a direct contribution of DUOX1 silencing to epithelial-to-mesenchymal transition (EMT), an important feature of metastatic cancer...
October 3, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27526110/systemic-chromosome-instability-in-shugoshin-1-mice-resulted-in-compromised-glutathione-pathway-activation-of-wnt-signaling-and-defects-in-immune-system-in-the-lung
#12
H Y Yamada, G Kumar, Y Zhang, E Rubin, S Lightfoot, W Dai, C V Rao
Mitotic error-mediated chromosome instability (CIN) can lead to aneuploidy, chromothripsis, DNA damage and/or whole chromosome gain/loss. CIN may prompt rapid accumulation of mutations and genomic alterations. Thus, CIN can promote carcinogenesis. This CIN process results from a mutation in certain genes or environmental challenge such as smoking, and is highly prevalent in various cancers, including lung cancer. A better understanding of the effects of CIN on carcinogenesis will lead to novel methods for cancer prevention and treatment...
August 15, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27526109/loss-of-the-oncogenic-phosphatase-prl-3-promotes-a-tnf-r1-feedback-loop-that-mediates-triple-negative-breast-cancer-growth
#13
H H Gari, G D DeGala, M S Lucia, J R Lambert
Stimulating tumor cell senescence and apoptosis are proven methods for therapeutically combating cancer. However, senescence and apoptosis are conventionally viewed as parallel, not sequential, processes. We have discovered that the metastasis-promoting phosphatase, PRL-3, is transcriptionally regulated by the NF-ĸB pathway in triple-negative breast cancer (TNBC) cells, and that PRL-3 knockdown elicits an autocrine tumor necrosis factor receptor 1 (TNF-R1) feedback loop that results in TNBC cell senescence followed by apoptosis...
August 15, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27526105/targeting-src-in-endometriosis-associated-ovarian-cancer
#14
R Manek, E Pakzamir, P Mhawech-Fauceglia, T Pejovic, H Sowter, S A Gayther, K Lawrenson
The SRC proto-oncogene is commonly overexpressed or activated during cancer development. Src family kinase inhibitors are approved for the treatment of certain leukemias, and are in clinical trials for the treatment of solid tumors. Src signaling is activated in endometriosis, a precursor of clear cell and endometrioid subtypes of epithelial ovarian cancers (OCs). We examined the expression of phosphorylated Src (Src-pY416) in 381 primary OC tissues. Thirty-six percent of OCs expressed Src-pY416. Src-pY416 expression was most common in endometriosis-associated OCs (EAOCs) (P=0...
August 15, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27500388/modification-of-tumor-cell-exosome-content-by-transfection-with-wt-p53-and-microrna-125b-expressing-plasmid-dna-and-its-effect-on-macrophage-polarization
#15
M Trivedi, M Talekar, P Shah, Q Ouyang, M Amiji
Exosomes are responsible for intercellular communication between tumor cells and others in the tumor microenvironment. These microvesicles promote oncogensis and can support towards metastasis by promoting a pro-tumorogenic environment. Modifying the exosomal content and exosome delivery are emerging novel cancer therapies. However, the clinical translation is limited due to feasibility of isolating and delivery of treated exosomes as well as an associated immune response in patients. In this study, we provide proof-of-concept for a novel treatment approach for manipulating exosomal content by genetic transfection of tumor cells using dual-targeted hyaluronic acid-based nanoparticles...
August 8, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27454080/comparative-transcriptomic-analysis-reveals-the-oncogenic-fusion-protein-pax3-foxo1-globally-alters-mrna-and-mirna-to-enhance-myoblast-invasion
#16
J M Loupe, P J Miller, B P Bonner, E C Maggi, J Vijayaraghavan, J S Crabtree, C M Taylor, J Zabaleta, A D Hollenbach
Rhabdomyosarcoma, one of the most common childhood sarcomas, is comprised of two main subtypes, embryonal and alveolar (ARMS). ARMS, the more aggressive subtype, is primarily characterized by the t(2;13)(p35;p14) chromosomal translocation, which fuses two transcription factors, PAX3 and FOXO1 to generate the oncogenic fusion protein PAX3-FOXO1. Patients with PAX3-FOXO1-postitive tumors have a poor prognosis, in part due to the enhanced local invasive capacity of these cells, which leads to the increased metastatic potential for this tumor...
July 25, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27294866/loss-of-olfm4-promotes-tumor-migration-through-inducing-interleukin-8-expression-and-predicts-lymph-node-metastasis-in-early-gastric-cancer
#17
J Zhao, P Shu, F Duan, X Wang, L Min, Z Shen, Y Ruan, J Qin, Y Sun, X Qin
Endoscopic surgery is increasingly used for early gastric cancer (EGC) treatment worldwide, and lymph node metastasis remains the most important risk factor for endoscopic surgery in EGC patients. Olfactomedin 4 (OLFM4) is mainly expressed in the digestive system and upregulated in several types of tumors. However, the role of OLFM4 in EGC has not been explored. We evaluated OLFM4 expression by immunohistochemical staining in 105 patients with EGC who underwent gastrectomy. The clinicopathological factors and OLFM4 expression were co-analyzed to predict lymph node metastasis in EGC...
June 13, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27270613/nik-regulates-mt1-mmp-activity-and-promotes-glioma-cell-invasion-independently-of-the-canonical-nf-%C3%AE%C2%BAb-pathway
#18
C L Duran, D W Lee, J-U Jung, S Ravi, C B Pogue, L G Toussaint, K J Bayless, R Sitcheran
A growing body of evidence implicates the noncanonical NF-κB pathway as a key driver of glioma invasiveness and a major factor underlying poor patient prognoses. Here, we show that NF-κB-inducing kinase (NIK/MAP3K14), a critical upstream regulator of the noncanonical NF-κB pathway, is both necessary and sufficient for cell-intrinsic invasion, as well as invasion induced by the cytokine TWEAK, which is strongly associated with tumor pathogenicity. NIK promotes dramatic alterations in glioma cell morphology that are characterized by extensive membrane branching and elongated pseudopodial protrusions...
June 6, 2016: Oncogenesis
https://www.readbyqxmd.com/read/26900952/understanding-cachexia-as-a-cancer-metabolism-syndrome
#19
REVIEW
P E Porporato
Metabolic reprogramming occurs in tumors to foster cancer cell proliferation, survival and metastasis, but as well at a systemic level affecting the whole organism, eventually leading to cancer cachexia. Indeed, as cancer cells rely on external sources of nitrogen and carbon skeleton to grow, systemic metabolic deregulation promoting tissue wasting and metabolites mobilization ultimately supports tumor growth. Cachectic patients experience a wide range of symptoms affecting several organ functions such as muscle, liver, brain, immune system and heart, collectively decreasing patients' quality of life and worsening their prognosis...
February 22, 2016: Oncogenesis
https://www.readbyqxmd.com/read/27617643/zeb1-induces-epb41l5-in-the-cancer-mesenchymal-program-that-drives-arf6-based-invasion-metastasis-and-drug-resistance
#20
A Hashimoto, S Hashimoto, H Sugino, A Yoshikawa, Y Onodera, H Handa, T Oikawa, H Sabe
Onset of the cancer mesenchymal program is closely associated with cancer malignancy and drug resistance. Among the different epithelial-mesenchymal transition (EMT)-associated transcriptional factors, ZEB1 has a key role in inducing the mesenchymal phenotypes and stem cell-like properties of different breast cancer cells. ARF6 and its effector AMAP1 are frequently overexpressed in breast cancer cells, and promote invasion, metastasis and drug resistance. EPB41L5 is induced during EMT, and mediates the disruption of E-cadherin-based cell-cell adhesion and the promotion of focal adhesion dynamics...
2016: Oncogenesis
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