Добірка наукової літератури з теми "Anchorage-independent cell growth"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Anchorage-independent cell growth".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Anchorage-independent cell growth"
Macintyre, John, David D. Hume, Janet Smith, and John C. McLachlan. "A microwell assay for anchorage independent cell growth." Tissue and Cell 20, no. 3 (January 1988): 331–38. http://dx.doi.org/10.1016/0040-8166(88)90068-7.
Повний текст джерелаAdam, Rosalyn M., Stephen G. Chamberlin, and Donna E. Davies. "Induction of Anchorage-Independent Growth by Amphiregulin." Growth Factors 13, no. 3-4 (January 1996): 193–203. http://dx.doi.org/10.3109/08977199609003221.
Повний текст джерелаZhu, Xiaoyun, Eric Scharf та Richard K. Assoian. "Induction of Anchorage-independent Growth by Transforming Growth Factor-β Linked to Anchorage-independent Expression of Cyclin D1". Journal of Biological Chemistry 275, № 10 (10 березня 2000): 6703–6. http://dx.doi.org/10.1074/jbc.275.10.6703.
Повний текст джерелаQu, Jian, Marta S. Cammarano, Qing Shi, Kenneth C. Ha, Primal de Lanerolle, and Audrey Minden. "Activated PAK4 Regulates Cell Adhesion and Anchorage-Independent Growth." Molecular and Cellular Biology 21, no. 10 (May 15, 2001): 3523–33. http://dx.doi.org/10.1128/mcb.21.10.3523-3533.2001.
Повний текст джерелаHuseinovic, Angelina, Annelieke Jaspers, Annina P. van Splunter, Hanne Sørgård, Saskia M. Wilting, Dorian R. A. Swarts, Ida H. van der Meulen, Victor W. van Beusechem, Renée X. de Menezes, and Renske D. M. Steenbergen. "Functional Screen for microRNAs Suppressing Anchorage-Independent Growth in Human Cervical Cancer Cells." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4791. http://dx.doi.org/10.3390/ijms23094791.
Повний текст джерелаGuadagno, T. M., and R. K. Assoian. "G1/S control of anchorage-independent growth in the fibroblast cell cycle." Journal of Cell Biology 115, no. 5 (December 1, 1991): 1419–25. http://dx.doi.org/10.1083/jcb.115.5.1419.
Повний текст джерелаYang, Jaw-Ji, Jong-Sun Kang, and Robert S. Krauss. "Ras Signals to the Cell Cycle Machinery via Multiple Pathways To Induce Anchorage-Independent Growth." Molecular and Cellular Biology 18, no. 5 (May 1, 1998): 2586–95. http://dx.doi.org/10.1128/mcb.18.5.2586.
Повний текст джерелаHalatsch, Marc-Eric, Esther E. Gehrke, Vassilios I. Vougioukas, Ingolf C. Bötefür, Farhad A.-Borhani, Thomas Efferth, Erich Gebhart, Sebastian Domhof, Ursula Schmidt, and Michael Buchfelder. "Inverse correlation of epidermal growth factor receptor messenger RNA induction and suppression of anchorage-independent growth by OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in glioblastoma multiforme cell lines." Journal of Neurosurgery 100, no. 3 (March 2004): 523–33. http://dx.doi.org/10.3171/jns.2004.100.3.0523.
Повний текст джерелаHalatsch, Marc-Eric, Esther E. Gehrke, Vassilios I. Vougioukas, Ingolf C. Bötefür, Farhad A. Borhani, Thomas Efferth, Erich Gebhart, Sebastian Domhof, Ursula Schmidt, and Michael Buchfelder. "Inverse correlation of epidermal growth factor receptor messenger RNA induction and suppression of anchorage-independent growth by OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in glioblastoma multiforme cell lines." Neurosurgical Focus 16, no. 2 (February 2004): 1–11. http://dx.doi.org/10.3171/foc.2004.16.2.12.
Повний текст джерелаHan, EK, TM Guadagno, SL Dalton, and RK Assoian. "A cell cycle and mutational analysis of anchorage-independent growth: cell adhesion and TGF-beta 1 control G1/S transit specifically." Journal of Cell Biology 122, no. 2 (July 15, 1993): 461–71. http://dx.doi.org/10.1083/jcb.122.2.461.
Повний текст джерелаДисертації з теми "Anchorage-independent cell growth"
Moore, Sarah Margaret. "Phosphoinositide 3-kinase regulation of anchorage-independent growth and drug resistance in small cell lung cancer cells." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/21429.
Повний текст джерелаLawson, Erika Lynn. "The transmembrane domain of CEACAM1a-4S is a determinant of anchorage independent growth and tumorigenicity." View abstract/electronic edition; access limited to Brown University users, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3319101.
Повний текст джерелаAndrews, Natalie M. "Beta1 integrin modulates the anchorage independent growth, invasion and migration of prostate cancer cell line PC3." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28850.
Повний текст джерелаSaulnier, Ronald B. "The role of extracellular matrix and growth factors in anchorage-independent growth of a mouse mammary carcinoma cell line." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq20587.pdf.
Повний текст джерелаHoneywell, David R. "The Effect of hsa-miR-105 on Prostate Cancer Growth." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23578.
Повний текст джерелаShukla, Madhura Shirish. "Role of PERK in Anchorage-Independent Growth of Colorectal Carcinoma and Cell Migration In-Vitro." Thesis, 2020. http://hdl.handle.net/1805/24082.
Повний текст джерелаThe unfolded protein response (UPR) is important for cell adaptation to accumulation of unfolded proteins in the endoplasmic reticulum (ER). A central UPR sensor of ER stress is PKR- like ER Kinase (PERK), which phosphorylates eIF2 to reduce global translation and help mitigate ER stress. While this is a survival mechanism that serves to save the cell from catastrophic events during ER stress, PERK can also be activated in cancer cells due to genetic changes and exposure to stresses inherent in the tumor micro-environment. Published reports have indicated that PERK is activated in cancer cells in response to hypoxia, nutrient deprivation, matrix detachment, and increased protein load by oncogene activation to facilitate cell survival. The UPR features PERK and another ER stress sensory protein, IRE1α, which also regulates the dynamic assembly of the actin cytoskeleton; loss of either PERK or IRE1α functions decrease cell migration activity. We hypothesized that PERK is required for anchorage-independent survival of the cancer cell line HCT116 and that PERK is essential for cell migration. Consistent with these premises, inhibition of PERK using pharmacological inhibitors GSK2656157 and LY-4 in suspended cells showed reduced growth. Furthermore, PERK-deficient cells showed reduced migration in transwell migration assays as compared to their wild type counterpart. These results suggest that PERK facilitates anchorage-independent growth of cancer cells and cell migration.
De, la Mare Jo-Anne, Tamarin Jurgens, and Adrienne Lesley Edkins. "Extracellular Hsp90 and TGFP regulate adhesion, migration and anchorage independent growth in a paired colon cancer cell line model." 2017. http://hdl.handle.net/10962/59920.
Повний текст джерелаWei-EnChang and 張瑋恩. "The Role of Thrombomodulin in Modulating Anchorage-independent Growth of Tumor Cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/50394818464963125894.
Повний текст джерела國立成功大學
醫學檢驗生物技術學系碩博士班
98
Thrombomodulin (TM), a type I transmembrane glycoprotein plays important roles in cell adhesion and tumorigenesis. Tumorigenesis is a complicated process including angiogenesis and metastasis. Anchorage-independent growth has been recognized as a hallmark of cell transformation which promotes tumor metastasis. Increase of soluble TM was found in plasma of cancer patients; however, the biological function of soluble TM remains unclear. Moreover, rhomboid, an intramembrane protease specifically cleaves TM at its transmembrane domain, and cause release of soluble TM from cell membrane. In this study, we investigated whether soluble TM promotes anchorage-independent growth in tumor cells. Human cervical cancer cell lines formed colonies in soft agar and survived until day 14th. Lentivirus transduction of short hairpin RNA was used to knockdown TM expression in HeLa229 cells (HeLa229-shTM), and the efficiency of TM knockdown was confirmed by Western blotting. HeLa229-shTM showed lower colony numbers and smaller size in suspension culture. Moreover, knockdown of TM in HeLa229 decreased extracellular signal regulated kinase phosphorylation and increased caspase 3 activation compared with vector control (HeLa229-shLuc). The level of rhomboid was upregulated in HeLa229-shLuc in suspension culture for 24 and 48 hour; however, TM-knockdown cells had no such effect. After treatment with dichloroisocoumarin, a rhomboid inhibitor, the levels of soluble TM and ERK phosphorylation were decreased. Recombinant TM domains 1, 2 and 3 increased cell viability, ERK phosphorylation and decreased caspase 3 activation in suspension. In summary, TM was shedded by rhomboid, and soluble TM promoted anchorage-independent growth of tumor cells.
Tsai, Wen-Chuan, and 蔡文娟. "Effects of Ha-ras oncogene and growth factors on anchorage- independent growth of 212 cells." Thesis, 1995. http://ndltd.ncl.edu.tw/handle/99431888375045616539.
Повний текст джерела國立成功大學
微生物及免役學研究所
83
The effects of Ha-ras oncogene and related factors on anchorage- independent growth of a212 cell line derived from NIH3T3 cells in soft agar was investigated. The 212 cell contains an inducible Ha-ras oncogene which is under the control of Escherichia coli lactose regulatory elements. When cells were maintained in soft agar containing 10% calf serum, overexpression of Ha-ras oncogene stimulated colony formation. When cells were cultured in soft agar containing only 0.2% calf serum, no colony was detected even with IPTG induction, indicating that besides activated Ha-ras oncogene , some factor( s) in serum are also required for anchorage- indenpendent growth. However, simply adding anchorage- independent growth related growth factors (EGF, PDGF, bFGF, Insulin or IGF-1) into soft agar containing 0.2% calf serum could not induce colony formation. While 0.2% calf serum was replaced with bovine colostrum (AC-2 , Valio, Finland) to compensate nutrient inadequacy, the characteristic of unable to form colony remained, indicating that AC-2 either contains inhibitors or lacks the factor(s) for anchorage- independent growth. So far no inhibitor was detected in AC-2, and diverse levels of colony formation were stimulated by growth factors except TGF-b1 in AC-2 containing medium with IPTG induction. Calf serum was separated by gel filtration into 4 fractions, and each fraction was added into AC-2 containing medium with IPTG induction. The 4th fraction could stimulate cell colony formation, and its molecular weight is smaller than 14 Kd. When we added the inhibitors (lovastatin and pravastatin) of Ras oncoprotein, colony formation efficiency declined. When anti-IGF-1 receptor antibody was added (which block the signal pathway of IGF-1 ), colony formation was also inhibited. Again these data suggest that at least two pathways are required for anchorage- independent growth : one is ras pathway, and IGF-1 is one of the other pathways.
Yang, Tian-Ren, and 楊天仁. "Overexpression of miR-10b and miR-20b promotes anchorage-independent growth and invasion in human colon cancer COLO320DM cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/42320820059891980941.
Повний текст джерела中山醫學大學
醫學研究所
102
Objective:The objective of this study is to understand the relation of different subtype (adhesion and suspension) in colon cancer cell line, COLO320DM between the miR express that might change cancer property. Methods and Materials:In primary data, we find when miR-10b and miR-20b overexpression COLO320DM will grow in suspension type. Then, we design experiences, including cell growth of COLO320 DM, anchorage-dependent growth of colon cancer cell lines, cell adhesive ability to ECM, the difference of migratory and invasive activity, drug sensitivity of chemotherapy drug 5-FU, expression of cancer stem cell markers, the expressed levels of AKT, GSK3β and ERK, the levels of intracellular ROS, the expressed levels of antioxidative enzymes, antioxidative enzyme activity to prove whether cell malignant property change. Results:The results shows COLO320DM cell grows in suspended type while miR-10b and miR-20b overexpress. And COLO320DM cell grow in adhesive type while miR-10b and miR-20b express low. In normal culture environment, suspended COLO320DM cell growth rate is faster than adhesive COLO320DM cell. In anchorage-independent surrounding, suspended COLO320DM cell growth rate is faster than adhesive COLO320DM cell. And cell adhesive ability of ECM molecules, suspended COLO320DM cell is stronger than adhesive COLO320DM cell. The resistant ability of chemotherapy drug, 5-FU suspended COLO320DM cell is higher than adhesive COLO320DM cell. The expression of p-AKTS473 and p-AKTT308 is suspended COLO320DM cell is higher than adhesive COLO320DM cell. The cancer stem cell containing have on difference between this two cell types. And expression of antioxidant enzyme are that catalase and glutathione peroxidase expression are adhesive COLO320DM cell higher than suspended COLO320DM cell. The activation of glutathione peroxidase is adhesive COLO320DM cell higher than suspended COLO320DM cell. The glutathione containing is suspended COLO320DM cell is higher than adhesive COLO320DM cell. Conclusion:In colon cancer, miR-10b and miR-20b are oncomir. When miR-10b and miR-20b overexpresses, malignancy (cell growth rate, migratory ability, invasive ability, resistant of chemotherapy drug 5-FU) of colon cancer will increase. But the real function and the mechanism of downstream molecules needs more study to solve. And our study is not using inhibitor to knockdown expression of miR-10b and miR-20b. The other is not using animal model to know growth rate in xenograft.
Частини книг з теми "Anchorage-independent cell growth"
Wang, Shunyou. "Anchorage-Independent Growth of Prostate Cancer Stem Cells." In Methods in Molecular Biology, 151–60. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9_9.
Повний текст джерелаGoto, Takehiko, Hiroyuki Honda, Naohiro Shiragami, and Hajime Unno. "Growth of Anchorage-Independent Animal Cells Captured in Newly Developed Porous Microcarriers." In Biochemical Engineering for 2001, 350–52. Tokyo: Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-68180-9_93.
Повний текст джерела"Anchorage-Independent Cell Growth." In Encyclopedia of Cancer, 173. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_262.
Повний текст джерелаToole, Bryan P., Rebecca M. Peterson, and Shibnath Ghatak. "INHIBITION OF TUMOR GROWTH IN VIVO AND ANCHORAGE-INDEPENDENT GROWTH IN VITRO BY PERTURBING HYALURONAN-CELL INTERACTIONS." In Hyaluronan, 349–54. Elsevier, 2002. http://dx.doi.org/10.1533/9781845693121.349.
Повний текст джерелаCentonze, Giorgia, Jennifer Chapelle, Costanza Angelini, Dora Natalini, Davide Cangelosi, Vincenzo Salemme, Alessandro Morellato, Emilia Turco, and Paola Defilippi. "The Scaffold Protein p140Cap as a Molecular Hub for Limiting Cancer Progression: A New Paradigm in Neuroblastoma." In Pheochromocytoma, Paraganglioma and Neuroblastoma. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96383.
Повний текст джерелаHamburger, Anne W. "Stimulation of Anchorage-Independent Growth of Human Tumor Cells by Macrophages." In Growth Regulation and Carcinogenesis, 87–92. CRC Press, 2020. http://dx.doi.org/10.1201/9781351072311-9.
Повний текст джерелаТези доповідей конференцій з теми "Anchorage-independent cell growth"
Barnard, Rebecca A., Paola Maycotte, Ryan J. Hansen, Daniel L. Gustafson, and Andrew Thorburn. "Abstract C19: The effect of autophagy inhibition on anchorage-independent cell growth." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-c19.
Повний текст джерелаSato, Mitsuo, Yoshihiro Takeyama, Mihoko Horio, Tetsunari Hase, Kenya Yoshida, Harunori Nakashima, Naozumi Hashimoto, et al. "Abstract 2295: Knockdown ofZEB1, a master EMT gene, suppresses anchorage-independent cell growth of lung cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2295.
Повний текст джерелаJiang, Lei, Alexander Shestov, Lance S. Terada, Nicholas D. Adams, Michael T. McCabe, Beth Pietrak, Stan J. Schimidt, Benjamin Schwartz, and Ralph J. DeBerardinis. "Abstract A35: Cytosolic reductive carboxylation is required for mitochondrial redox homeostasis during anchorage-independent cell growth." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a35.
Повний текст джерелаGuin, Sunny, and Craig Richmond. "Abstract 3449: AGL loss promotes anchorage independent growth of non-small cell lung cancer by activating FAK." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3449.
Повний текст джерелаGoydos, James S., Negar M. Salehomoum, Steve Rosenberg, Joseph L.-K. Chan, and Yu Wen. "Abstract LB-40: Inhibition of anchorage-independent growth of melanoma cell lines using Riluzole in combination with PI3 kinase pathway inhibitors." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-40.
Повний текст джерелаLiao, Xin, Chao Huang, Jingxia Li, and Chuanshu Huang. "Abstract 533: XIAP BIR domain suppresses miR-200a expression and subsequently promotes EGFR protein translation and anchorage-independent growth of bladder cancer cell." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-533.
Повний текст джерелаGoldenberg, DM, Y. Wang, P. Trisal, TM Cardillo, EA Rossi, and C.-H. Chang. "P3-02-01: A Novel Bispecific, Hexavalent, Antibody (HexAb) Inhibits Anchorage-Independent Growth and Reduces Invasiveness of Triple-Negative Breast Cancer Cell Lines In Vitro." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-02-01.
Повний текст джерелаWang, Yang, Pretti Trisal, Thomas M. Cardillo, Ed Rossi, David M. Goldenberg, and Chien-Hsing Chang. "Abstract 2727: Bispecific, hexavalent antibodies (HexAbs) targeting IGF-1R and either Trop-2 or CEACAM6 inhibit anchorage-independent growth and invasion of antigen-expressing breast and pancreatic cancer cell linesin vitro." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2727.
Повний текст джерелаVanderVeen, Nathan T., Nicholas Raja, Elizabeth Yi, James Curtin, Peter Chockley, Hikmat Assi, Jonathan Savakus, et al. "Abstract 3195: STAT3 inhibition using shRNA inhibits GBM proliferation, cell migration, anchorage-independent growth of mouse, rat, and human stem-like cells in vitro; and it induces long term survival and anti-GBM immunity in vivo." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3195.
Повний текст джерелаRotem, Asaf, Benjamin Izar, and Levi A. Garraway. "Abstract 600: Melanoma and ovarian cancer cells tested for drug sensitivity using anchorage-independent growth." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-600.
Повний текст джерела