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Corinne N Haines, Kara M Braunreiter, Xiaokui Molly Mo, and Craig J Burd

-dependent breast cancer, the activation of ERα ultimately leads to proliferation ( Dixon 2014 ). ER-positive breast cancers are treated with endocrine therapies that disrupt the activity of ERα ( Heldring et al . 2007 ). Unfortunately, patients develop resistance

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Douglas A Gibson, Frances Collins, Fiona L Cousins, Arantza Esnal Zufiaurre, and Philippa T K Saunders

. 2016 ). Obesity is a major modifiable risk factor for EC and is thought to contribute to increased risk of malignancy in part due to increased exposure to estrogens, which enhance the risk of aberrant proliferation within the endometrium ( Sanderson et

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M Principe, M Chanal, V Karam, A Wierinckx, I Mikaélian, R Gadet, C Auger, V Raverot, E Jouanneau, A Vasiljevic, A Hennino, G Raverot, and P Bertolino

instance, BMP4 is capable of stimulating the proliferation of GH3 cells, a rat prolactinoma-derived cell line ( Paez-Pereda et al . 2003 ), whereas TGFβ inhibits this effect and is further capable of repressing prolactin expression in both GH3 and GH4

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Kathrin A Schmohl, Yang Han, Mariella Tutter, Nathalie Schwenk, Rim S J Sarker, Katja Steiger, Sibylle I Ziegler, Peter Bartenstein, Peter J Nelson, and Christine Spitzweg

expression of TRs have been described in many different human cancers. TRβ is generally believed to act as a tumour suppressor and was shown to decrease cancer cell proliferation and invasiveness, while downregulation of TRβ seems to increase cell

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Thomas Tawadros, Florian Alonso, Patrice Jichlinski, Noel Clarke, Thierry Calandra, Jacques-Antoine Haefliger, and Thierry Roger

( Calandra & Roger 2003 , Calandra et al . 2003 ). Additionally, MIF functions in many oncogenic processes including cell proliferation, angiogenesis and suppression of host–tumour cell immune surveillance ( Mitchell 2004 , Bucala & Donnelly 2007 ). MIF is

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Salma Ben-Salem, Varadha Balaji Venkadakrishnan, and Hannelore V Heemers

and mechanisms of treatment resistance remain unknown. Deregulated cell proliferation has been recognized as the minimal common platform upon which all neoplastic evolution occurs. Cell proliferation is tightly regulated by orderly transitions

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Zhe Wang, Ke Ma, Steffie Pitts, Yulan Cheng, Xi Liu, Xiquan Ke, Samuel Kovaka, Hassan Ashktorab, Duane T Smoot, Michael Schatz, Zhirong Wang, and Stephen J Meltzer

functional assays using interference and overexpression of circNF1 revealed that circNF1 promotes cell proliferation. Finally, circNF1 functioned as a miR-16 sponge, derepressing the miR-16 target genes MAP7 and AKT3 . We conclude that circNF1

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Veronica Kalhori, Melissa Magnusson, Muhammad Yasir Asghar, Ilari Pulli, and Kid Törnquist

substantial amount of evidence has implicated S1P in the progression of several types of cancers by enhancing many central events such as proliferation, angiogenesis, migration, and invasion ( Alvarez et al . 2007 , Strub et al . 2010 , Alshaker et al

Open access

Julia Hoefer, Johann Kern, Philipp Ofer, Iris E Eder, Georg Schäfer, Dimo Dietrich, Glen Kristiansen, Stephan Geley, Johannes Rainer, Eberhard Gunsilius, Helmut Klocker, Zoran Culig, and Martin Puhr

.5 μg/six wells) using 3 μl of Fugene HD (Roche) for 48 h. For stable overexpression, the cells were selected with 0.5 mg/ml of G418 (neomycin) for 7 days. Proliferation measurement Proliferation was assessed using [ 3 H]thymidine incorporation assay as

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Yoshiaki Onodera, Hozumi Motohashi, Kiyoshi Takagi, Yasuhiro Miki, Yukiko Shibahara, Mika Watanabe, Takanori Ishida, Hisashi Hirakawa, Hironobu Sasano, Masayuki Yamamoto, and Takashi Suzuki

the blots were detected using ECL-Plus Western Blotting Detection Reagents (GE Healthcare), and the protein bands were visualized using an LAS-1000 image analyzer (Fuji Photo Film, Tokyo, Japan). Cell proliferation and migration assays One day after