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Emt cancer initiation

Vincent Le Coz, Chaobin Zhu, Aurore Devocelle, Aimé Vazquez, Claude Boucheix, Sandy Azzi, Cindy Gallerne, Pierre Eid, Séverine Lecourt, Julien Giron-Michel
Melanoma is a particularly virulent human cancer, due to its resistance to conventional treatments and high frequency of metastasis. Melanomas contain a fraction of cells, the melanoma-initiating cells (MICs), responsible for tumor propagation and relapse. Identification of the molecular pathways supporting MICs is, therefore, vital for the development of targeted treatments. One factor produced by melanoma cells and their microenvironment, insulin-like growth factor-1 (IGF- 1), is linked to epithelial-mesenchymal transition (EMT) and stemness features in several cancers...
October 18, 2016: Oncotarget
Kishore Polireddy, Ruochen Dong, Peter R McDonald, Tao Wang, Brendan Luke, Ping Chen, Melinda Broward, Anuradha Roy, Qi Chen
BACKGROUND: Pancreatic cancer has an enrichment of stem-like cancer cells (CSCs) that contribute to chemoresistant tumors prone to metastasis and recurrence. Drug screening assays based on cytotoxicity cannot identify specific CSC inhibitors, because CSCs comprise only a small portion of cancer cell population, and it is difficult to propagate stable CSC populations in vitro for high-throughput screening (HTS) assays. Based on the important role of cancer cell epithelial-to-mesenchymal transition (EMT) in promoting CSCs, we hypothesized that inhibition of EMT can be a useful strategy for inhibiting CSCs, and therefore a feasible approach for HTS can be built for identification of CSC inhibitors, based on assays detecting EMT inhibition...
2016: PloS One
Tao Yin, Guoping Wang, Sisi He, Guobo Shen, Chao Su, Yan Zhang, Xiawei Wei, Tinghong Ye, Ling Li, Shengyong Yang, Dan Li, Fuchun Guo, Zemin Mo, Yang Wan, Ping Ai, Xiaojuan Zhou, Yantong Liu, Yongsheng Wang, Yuquan Wei
Malignant pleural effusion (PE) and ascites, common clinical manifestations in advanced cancer patients, are associated with poor prognosis. However, the biological characteristics of malignant PE and ascites are not clarified. Here, we report that malignant PE and ascites can induce frequent epithelial-mesenchymal transition (EMT) program and endow tumor cells with stem cell properties with high efficiency, which promote tumor growth, chemoresistance and immune evasion. We determine that this EMT process is mainly dependent on VEGF, one initiator of PI3K/Akt/mTOR pathway...
October 18, 2016: Journal of Biological Chemistry
Shuitu Feng, Zhigao Zheng, Lihua Feng, Lihong Yang, Zuhong Chen, Yubiao Lin, Yingqin Gao, Yide Chen
The cancer stem cell (CSC) model suggests that a small subset of cancer cells possess stem cell properties and plays a crucial role in tumor initiation, metastasis and resistance to anticancer therapy. Exploration of the specific therapies targeting at CSCs has been a crucial issue in antitumor research. Gastric cancer (GC) cells often exist in an ischemic microenvironment with acidic conditions in vivo, thus maintenance of cellular pH homeostasis is important for the survival and function of GC cells. Proton pump inhibitors (PPIs) may prevent intracellular proton extrusions which consequently reduce cancer cell survival under acidic conditions...
October 7, 2016: Oncology Reports
Bhumika Wadhwa, Rashmi Dumbre
Prostate (CaP) cancer is the second-leading cause of cancer-related mortality in men in Western societies. Androgen receptor (AR) signaling is a critical survival pathway for prostate cancer cells, and androgen-deprivation therapy (ADT) remains the principal treatment for patients with locally advanced and metastatic disease. Although a majority of patients initially respond to ADT, most will eventually develop castrate resistance. The recent discovery that AR signaling persists during systemic castration via intratumoral production of androgens led to the development of novel anti-androgen therapies...
October 6, 2016: Chemico-biological Interactions
Zhongwei Li, Pingfu Hou, Dongmei Fan, Meichen Dong, Musong Ma, Hongyuan Li, Ruosi Yao, Yuxin Li, Guannan Wang, Pengyu Geng, Adhanom Mihretab, Dongxu Liu, Yu Zhang, Baiqu Huang, Jun Lu
EZH2 (the Enhancer of Zeste Homolog 2), as a key epigenetic regulator and EMT inducer, participates in a variety of cancer metastasis. EZH2 stability is regulated by several types of post-translational modifications (PTMs).The long non-coding RNAs (lncRNA) have been implicated to have critical roles in multiple carcinogenesis through a wide range of mechanisms, including modulating the stability of proteins. To date, whether the stability of EZH2 protein is regulated by lncRNAs remains unexplored. Here we report the discovery of ANCR modulating the stability of EZH2, and hence in the invasion and metastasis of breast cancer cells...
October 7, 2016: Cell Death and Differentiation
Hai-Ting Liu, Peng Gao
Metastasis is an important factor in predicting the prognosis of the patients with cancers and contributes to high cancer-related mortality. Recent studies indicated that microRNAs (miRNAs) played a functional role in the initiation and progression of human malignancies. MicroRNAs are small non-coding RNAs of about 22 nucleotides in length that can induce messenger RNA (mRNA) degradation or repress mRNA translation by binding to the 3' untranslated region (3'-UTR) of their target genes. Overwhelming reports indicated that miRNAs could regulate cancer invasion and metastasis via epithelial-to-mesenchymal transition (EMT)-related and/or non-EMT-related mechanisms...
October 6, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Giuseppina Sannino, Nicole Armbruster, Mona Bodenhöfer, Ursula Haerle, Diana Behrens, Malte Buchholz, Ulrich Rothbauer, Bence Sipos, Christian Schmees
Pancreatic ductal adenocarcinoma (PDAC) has a low overall survival rate, which is approximately 20% during the first year and decreases to less than 6% within five years of the disease. This is due to premature dissemination accompanied by a lack of disease-specific symptoms during the initial stages. Additionally, to date there are no biomarkers for an early prognosis available.A growing number of studies indicate that epithelial to mesenchymal transition (EMT), triggered by WNT-, TGF-β- and other signaling pathways is crucial for the initiation of the metastatic process in PDAC...
October 4, 2016: Oncotarget
Katharina Koch, Rudolf Hartmann, Friederike Schröter, Abigail Kora Suwala, Donata Maciaczyk, Andrea Caroline Krüger, Dieter Willbold, Ulf Dietrich Kahlert, Jaroslaw Maciaczyk
Glioblastoma (GBM) is the most malignant brain tumor with very limited therapeutic options. Standard multimodal treatments, including surgical resection and combined radio-chemotherapy do not target the most aggressive subtype of glioma cells, brain tumor stem cells (BTSCs). BTSCs are thought to be responsible for tumor initiation, progression, and relapse. Furthermore, they have been associated with the expression of mesenchymal features as a result of epithelial-mesenchymal transition (EMT) thereby inducing tumor dissemination and chemo resistance...
September 29, 2016: Oncotarget
Daniel F Milano, Robert J Natividad, Yasuhiro Saito, Catherine Y Luo, Senthil K Muthuswamy, Anand R Asthagiri
Epithelial-mesenchymal transition (EMT) is a complex process by which cells acquire invasive properties that enable escape from the primary tumor. Complete EMT, however, is not required for metastasis: circulating tumor cells exhibit hybrid epithelial-mesenchymal states, and genetic perturbations promoting partial EMT induce metastasis in vivo. An open question is whether and to what extent intermediate stages of EMT promote invasiveness. Here, we investigate this question, building on recent observation of a new invasive property...
October 4, 2016: Biophysical Journal
Matthias Ilmer, Nachman Mazurek, Michael Z Gilcrease, James C Byrd, Wendy A Woodward, Thomas A Buchholz, Kim Acklin, Karen Ramirez, Margarete Hafley, Eckhard Alt, Jody Vykoukal, Robert S Bresalier
BACKGROUND: Galectin-3 (Gal3) plays diverse roles in cancer initiation, progression, and drug resistance depending on tumor type characteristics that are also associated with cancer stem cells (CSCs). Recurrence of breast carcinomas may be attributed to the presence of breast CSCs (BCSCs). BCSCs exist in mesenchymal-like or epithelial-like states and the transition between these states endows BCSCs with the capacity for tumor progression. The discovery of a feedback loop with galectins during epithelial-to-mesenchymal transition (EMT) prompted us to investigate its role in breast cancer stemness...
September 29, 2016: Breast Cancer Research: BCR
Lisha Qi, Wangzhao Song, Lingmei Li, Lu Cao, Yue Yu, Chunmin Song, Yalei Wang, Fei Zhang, Yang Li, Bin Zhang, Wenfeng Cao
Several fibroblast growth factor (FGF) isoforms act to stimulate epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7 are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC) cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell morphology, promoted EMT-associated protein expression, and enhanced cell proliferation, migration/invasion and colony initiation. In addition, FGF4 increased store-operated calcium entry (SOCE) and expression of the calcium signal-associated protein Orai1...
September 22, 2016: Oncotarget
Jiawei Luo, Wei Huang, Buwen Cao
MicroRNAs (miRNAs) play an essential role in many biological processes by regulating the target genes, especially in the initiation and development of cancers. Therefore, the identification of the miRNA-mRNA regulatory modules is important for understanding the regulatory mechanisms. Most computational methods only used statistical correlations in predicting miRNA-mRNA modules, and neglected the fact there are causal relationships between miRNAs and their target genes. In this paper, we propose a novel approach called CALM(the causal regulatory modules) to identify the miRNA-mRNA regulatory modules through integrating the causal interactions and statistical correlations between the miRNAs and their target genes...
September 21, 2016: IEEE/ACM Transactions on Computational Biology and Bioinformatics
Miao Huang, Shengming Wu, Qiping Hu, Huayu Wu, Shu Wei, Huiqiong Xie, Kejian Sun, Xiaolong Li, Ling Fang
In our previous work, agkihpin, a snake venom arginine esterase (SVAE), was isolated from the Gloydius halys Pallas, which could attenuate the migration of liver cancer cells. However, the mechanism of the effect of agkihpin on attenuating migration of liver cancer cell is unknown yet. Here, to learn more about agkihpin and explore the possibility of agkihpin as an anti-metastatic drug in the future, a series of experiments about the migration and invasion of liver cancer cells with agkihpin, HepG 2 and SMMC-7721, was conducted...
October 14, 2016: Biochemical and Biophysical Research Communications
Jonathan Bergeman, Alexia Caillier, François Houle, Laurence M Gagné, Marc-Étienne Huot
By progressing through the epithelial to mesenchymal transition (EMT), cancer cells gain the ability to leave the primary tumor site and invade surrounding tissues. These metastatic cancers cells can further increase their plasticity by adopting an amoeboid-like morphology, by undergoing mesenchymal to amoeboid transition (MAT). We found that adhering cells producing spreading initiation centers (SIC), a transient structure localized above nascent adhesion complexes, share common biological and morphological characteristics associated with amoeboid cells...
September 16, 2016: Journal of Cell Science
Xiaolu Duan, Tao Zhang, Zhenzhen Kong, Xin Mai, Chuangxin Lan, Dong Chen, Yang Liu, Zhiwen Zeng, Chao Cai, Tuo Deng, Wenqi Wu, Guohua Zeng
Recently, β-arrestin1 was indicated as a tumor promoter in prostate cancer, but its exact role in cancer metastasis still have not been well clarified. Here, our data revealed that β-arrestin1 could promote the migration and invasion of prostate cancer cells via initiating epithelial-mesenchymal transition (EMT). Mechanically, β-arrestin1 could increase the transcriptional activity and expression of β-catenin, together with Akt activity, whereas decrease the activities of GSK-3β and PP2A. In addition, β-arrestin1 could function as a scaffold protein in modulating the interactions between PP2A, Akt, GSK-3β and β-catenin...
October 14, 2016: Biochemical and Biophysical Research Communications
Huocong Huang, Robert A Svoboda, Audrey J Lazenby, Jintana Saowapa, Nina Chaika, Ke Ding, Margaret J Wheelock, Keith R Johnson
Pancreatic ductal adenocarcinomas (PDAC) are highly malignant cancers characterized by extensive invasion into surrounding tissues, metastasis to distant organs, and a limited response to therapy. A main feature of PDAC is desmoplasia, which leads to extensive deposition of collagen I. We have demonstrated that collagen I can induce epithelial-mesenchymal transition (EMT) in pancreatic cancer cells. A hallmark of EMT is an increase in the expression of the mesenchymal cadherin N-cadherin. Previously we showed up-regulation of N-cadherin promotes tumor cell invasion and collagen I-induced EMT is mediated by two collagen receptors, alpha2beta1-integrin and discoidin domain receptor 1 (DDR1)...
September 7, 2016: Journal of Biological Chemistry
Geoffrey Richard, Stéphane Dalle, Marie-Ambre Monet, Maud Ligier, Amélie Boespflug, Roxane M Pommier, Arnaud de la Fouchardière, Marie Perier-Muzet, Lauriane Depaepe, Romain Barnault, Garance Tondeur, Stéphane Ansieau, Emilie Thomas, Corine Bertolotto, Robert Ballotti, Samia Mourah, Maxime Battistella, Céleste Lebbé, Luc Thomas, Alain Puisieux, Julie Caramel
Targeted therapies with MAPK inhibitors (MAPKi) are faced with severe problems of resistance in BRAF-mutant melanoma. In parallel to the acquisition of genetic mutations, melanoma cells may also adapt to the drugs through phenotype switching. The ZEB1 transcription factor, a known inducer of EMT and invasiveness, is now considered as a genuine oncogenic factor required for tumor initiation, cancer cell plasticity, and drug resistance in carcinomas. Here, we show that high levels of ZEB1 expression are associated with inherent resistance to MAPKi in BRAF(V)(600)-mutated cell lines and tumors...
October 4, 2016: EMBO Molecular Medicine
Marco Sciacovelli, Emanuel Gonçalves, Timothy Isaac Johnson, Vincent Roberto Zecchini, Ana Sofia Henriques da Costa, Edoardo Gaude, Alizee Vercauteren Drubbel, Sebastian Julian Theobald, Sandra Riekje Abbo, Maxine Gia Binh Tran, Vinothini Rajeeve, Simone Cardaci, Sarah Foster, Haiyang Yun, Pedro Cutillas, Anne Warren, Vincent Gnanapragasam, Eyal Gottlieb, Kristian Franze, Brian Huntly, Eamonn Richard Maher, Patrick Henry Maxwell, Julio Saez-Rodriguez, Christian Frezza
Mutations of the tricarboxylic acid cycle enzyme fumarate hydratase cause hereditary leiomyomatosis and renal cell cancer. Fumarate hydratase-deficient renal cancers are highly aggressive and metastasize even when small, leading to a very poor clinical outcome. Fumarate, a small molecule metabolite that accumulates in fumarate hydratase-deficient cells, plays a key role in cell transformation, making it a bona fide oncometabolite. Fumarate has been shown to inhibit α-ketoglutarate-dependent dioxygenases that are involved in DNA and histone demethylation...
August 31, 2016: Nature
Olga Karicheva, José Manuel Rodriguez-Vargas, Nadège Wadier, Kathline Martin-Hernandez, Romain Vauchelles, Najat Magroun, Agnès Tissier, Valérie Schreiber, Françoise Dantzer
Several members of the Poly(ADP-ribose) polymerase (PARP) family are essential regulators of genome integrity, actively prospected as drug targets for cancer therapy. Among them, PARP3 is well characterized for its functions in double-strand break repair and mitotis. Here we report that PARP3 also plays an integral role in TGFβ and reactive oxygen species (ROS) dependent epithelial-to-mesenchymal transition (EMT) and stem-like cell properties in human mammary epithelial and breast cancer cells. PARP3 expression is higher in breast cancer cells of the mesenchymal phenotype and correlates with the expression of the mesenchymal marker Vimentin while being in inverse correlation with the epithelial marker E-cadherin...
August 26, 2016: Oncotarget
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