Relevant bibliographies by topics / Anchorage-independent cell growth

Academic literature on the topic 'Anchorage-independent cell growth'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Anchorage-independent cell growth.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Anchorage-independent cell growth"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Adam, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Zhu, Xiaoyun, Eric Scharf, and 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, no. 10 (March 10, 2000): 6703–6. http://dx.doi.org/10.1074/jbc.275.10.6703.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Qu, 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.

Full text
Abstract:
ABSTRACT The serine/threonine kinase PAK4 is an effector molecule for the Rho GTPase Cdc42. PAK4 differs from other members of the PAK family in both sequence and function. Previously we have shown that an important function of this kinase is to mediate the induction of filopodia in response to activated Cdc42. Since previous characterization of PAK4 was carried out only with the wild-type kinase, we have generated a constitutively active mutant of the kinase to determine whether it has other functions. Expression of activated PAK4 in fibroblasts led to a transient induction of filopodia, which is consistent with its role as an effector for Cdc42. In addition, use of the activated mutant revealed a number of other important functions of this kinase that were not revealed by studying the wild-type kinase. For example, activated PAK4 led to the dissolution of stress fibers and loss of focal adhesions. Consequently, cells expressing activated PAK4 had a defect in cell spreading onto fibronectin-coated surfaces. Most importantly, fibroblasts expressing activated PAK4 had a morphology that was characteristic of oncogenic transformation. These cells were anchorage independent and formed colonies in soft agar, similar to what has been observed previously in cells expressing activated Cdc42. Consistent with this, dominant-negative PAK4 mutants inhibited focus formation by oncogenic Dbl, an exchange factor for Rho family GTPases. These results provide the first demonstration that a PAK family member can transform cells and indicate that PAK4 may play an essential role in oncogenic transformation by the GTPases. We propose that the morphological changes and changes in cell adhesion induced by PAK4 may play a direct role in oncogenic transformation by Rho family GTPases and their exchange factors.
APA, Harvard, Vancouver, ISO, and other styles
5

Huseinovic, 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.

Full text
Abstract:
The progression of anchorage-dependent epithelial cells to anchorage-independent growth represents a critical hallmark of malignant transformation. Using an in vitro model of human papillomavirus (HPV)-induced transformation, we previously showed that acquisition of anchorage-independent growth is associated with marked (epi)genetic changes, including altered expression of microRNAs. However, the laborious nature of the conventional growth method in soft agar to measure this phenotype hampers a high-throughput analysis. We developed alternative functional screening methods using 96- and 384-well ultra-low attachment plates to systematically investigate microRNAs regulating anchorage-independent growth. SiHa cervical cancer cells were transfected with a microRNA mimic library (n = 2019) and evaluated for cell viability. We identified 84 microRNAs that consistently suppressed growth in three independent experiments. Further validation in three cell lines and comparison of growth in adherent and ultra-low attachment plates yielded 40 microRNAs that specifically reduced anchorage-independent growth. In conclusion, ultra-low attachment plates are a promising alternative for soft-agar assays to study anchorage-independent growth and are suitable for high-throughput functional screening. Anchorage independence suppressing microRNAs identified through our screen were successfully validated in three cell lines. These microRNAs may provide specific biomarkers for detecting and treating HPV-induced precancerous lesions progressing to invasive cancer, the most critical stage during cervical cancer development.
APA, Harvard, Vancouver, ISO, and other styles
6

Guadagno, 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.

Full text
Abstract:
We have developed methodology to identify the block to anchorage-independent growth and position it within the fibroblast cell cycle. Results with NRK fibroblasts show that mitogen stimulation of the G0/G1 transition and G1-associated increases in cell size are minimally affected by loss of cell anchorage. In contrast, the induction of G1/S cell cycle genes and DNA synthesis is markedly inhibited when anchorage is blocked. Moreover, we demonstrate that the anchorage-dependent transition maps to late G1 and shortly before activation of the G1/S p34cdc2-like kinase. The G1/S block was also detectable in NIH-3T3 cells. Our results: (a) distinguish control of cell cycle progression by growth factors and anchorage; (b) indicate that anchorage mediates G1/S control in fibroblasts; and (c) identify a physiologic circumstance in which the phenotype of mammalian cell cycle arrest would closely resemble Saccharomyces cerevisiae START. The close correlation between anchorage independence in vitro and tumorigenicity in vivo emphasizes the key regulatory role for G1/S control in mammalian cells.
APA, Harvard, Vancouver, ISO, and other styles
7

Yang, 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.

Full text
Abstract:
ABSTRACT Several specific cell cycle activities are dependent on cell-substratum adhesion in nontransformed cells, and the ability of the Ras oncoprotein to induce anchorage-independent growth is linked to its ability to abrogate this adhesion requirement. Ras signals via multiple downstream effector proteins, a synergistic combination of which may be required for the highly altered phenotype of fully transformed cells. We describe here studies on cell cycle regulation of anchorage-independent growth that utilize Ras effector loop mutants in NIH 3T3 and Rat 6 cells. Stable expression of activated H-Ras (12V) induced soft agar colony formation by both cell types, but each of three effector loop mutants (12V,35S, 12V,37G, and 12V,40C) was defective in producing this response. Expression of all three possible pairwise combinations of these mutants synergized to induce anchorage-independent growth of NIH 3T3 cells, but only the 12V,35S-12V,37G and 12V,37G-12V,40C combinations were complementary in Rat 6 cells. Each individual effector loop mutant partially relieved adhesion dependence of pRB phosphorylation, cyclin E-dependent kinase activity, and expression of cyclin A in NIH 3T3, but not Rat 6, cells. The pairwise combinations of effector loop mutants that were synergistic in producing anchorage-independent growth in Rat 6 cells also led to synergistic abrogation of the adhesion requirement for these cell cycle activities. The relationship between complementation in producing anchorage-independent growth and enhancement of cell cycle activities was not as clear in NIH 3T3 cells that expressed pairs of mutants, implying the existence of either thresholds for these activities or additional requirements in the induction of anchorage-independent growth. Ectopic expression of cyclin D1, E, or A synergized with individual effector loop mutants to induce soft agar colony formation in NIH 3T3 cells, cyclin A being particularly effective. Taken together, these data indicate that Ras utilizes multiple pathways to signal to the cell cycle machinery and that these pathways synergize to supplant the adhesion requirements of specific cell cycle events, leading to anchorage-independent growth.
APA, Harvard, Vancouver, ISO, and other styles
8

Halatsch, 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.

Full text
Abstract:
Object. Quantitative and qualitative alterations in the epidermal growth factor receptor (EGFR) commonly occur in many cancers in humans, including malignant gliomas. The aim of the current study was to evaluate molecular and cellular effects of OSI-774, a novel EGFR tyrosine kinase inhibitor, on nine glioblastoma multiforme (GBM) cell lines. Methods. The effects of OSI-774 on expression of EGFR messenger (m)RNA and protein, proliferation, anchorage-independent growth, and apoptosis were examined using semiquantitative reverse transcription—polymerase chain reaction, immunocytochemical analysis, Coulter counting, soft agar cloning, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling/fluorescence-activated cell sorting, respectively. All p53 genes were completely and bidirectionally sequenced. Suppression of anchorage-independent growth by OSI-774 was inversely correlated to the induction of EGFR mRNA during relative serum starvation (r = −0.74) and was unrelated to p53 status. Overall, suppression of anchorage-independent growth was a considerably stronger effect of OSI-774 than inhibition of proliferation. The extent of OSI-774—induced apoptosis positively correlated with both proliferation and anchorage-independent growth of GBM cell lines (r = 0.75 and 0.79, respectively). In a single cell line derived from a secondary GBM, exposure to concentrations of greater than or equal to 1 Émol/L resulted in a substantial net cell loss during proliferation studies. Conclusions. The induction of EGFR mRNA may constitute a cellular mechanism to counteract the inhibitory effect of OSI-774 on the anchorage-independent growth of GBM cells. In contrast, no considerable correlation could be established between baseline expression levels of EGFR (both mRNA and protein) in GBM cell lines and their biological response to OSI-774. The OSI-774 induced greater (p53-independent) apoptosis in more malignant GBM phenotypes and may be a promising therapeutic agent against secondary GBM.
APA, Harvard, Vancouver, ISO, and other styles
9

Halatsch, 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.

Full text
Abstract:
Object Quantitative and qualitative alterations in the epidermal growth factor receptor (EGFR) commonly occur in many cancers in humans, including malignant gliomas. The aim of the current study was to evaluate molecular and cellular effects of OSI-774, a novel EGFR tyrosine kinase inhibitor, on nine glioblastoma multiforme (GBM) cell lines. Methods The effects of OSI-774 on expression of EGFR messenger (m)RNA and protein, proliferation, anchorage-independent growth, and apoptosis were examined using semiquantitative reverse transcription–polymerase chain reaction, immunocytochemical analysis, Coulter counting, soft agar cloning, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling/fluorescence-activated cell sorting, respectively. All p53 genes were completely and bidirectionally sequenced. Suppression of anchorage-independent growth by OSI-774 was inversely correlated to the induction of EGFR mRNA during relative serum starvation (r = −0.74) and was unrelated to p53 status. Overall, suppression of anchorage-independent growth was a considerably stronger effect of OSI-774 than inhibition of proliferation. The extent of OSI-774–induced apoptosis positively correlated with both proliferation and anchorage-independent growth of GBM cell lines (r = 0.75 and 0.79, respectively). In a single cell line derived from a secondary GBM, exposure to concentrations of greater than or equal to 1 μmol/L resulted in a substantial net cell loss during proliferation studies. Conclusions The induction of EGFR mRNA may constitute a cellular mechanism to counteract the inhibitory effect of OSI-774 on the anchorage-independent growth of GBM cells. In contrast, no considerable correlation could be established between baseline expression levels of EGFR (both mRNA and protein) in GBM cell lines and their biological response to OSI-774. The OSI-774 induced greater (p53-independent) apoptosis in more malignant GBM phenotypes and may be a promising therapeutic agent against secondary GBM.
APA, Harvard, Vancouver, ISO, and other styles
10

Han, 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.

Full text
Abstract:
We have examined cell cycle control of anchorage-independent growth in nontransformed fibroblasts. In previous studies using G0-synchronized NRK and NIH-3T3 cells, we showed that anchorage-independent growth is regulated by an attachment-dependent transition at G1/S that resembles the START control point in the cell cycle of Saccharomyces cerevisiae. In the studies reported here, we have synchronized NRK and NIH-3T3 fibroblasts immediately after this attachment-dependent transition to determine if other portions of the fibroblast cell cycle are similarly regulated by adhesion. Our results show that S-, G2-, and M-phase progression proceed in the absence of attachment. Thus, we conclude that the adhesion requirement for proliferation of these cells can be explained in terms of the single START-like transition. In related studies, we show that TGF-beta 1 overrides the attachment-dependent transition in NRK and AKR-2B fibroblasts (lines in which TGF-beta 1 induces anchorage-independent growth), but not in NIH-3T3 or Balb/c 3T3 fibroblasts (lines in which TGF-beta 1 fails to induce anchorage-independent growth). These results show that (a) adhesion and TGF-beta 1 can have similar effects in stimulating cell cycle progression from G1 to S and (b) the differential effects of TGF-beta 1 on anchorage-independent growth of various fibroblast lines are directly reflected in the differential effects of the growth factor at G1/S. Finally, we have randomly mutagenized NRK fibroblasts to generate mutant lines that have lost their attachment/TGF-beta 1 requirement for G1/S transit while retaining their normal mitogen requirements for proliferation. These clones, which readily proliferate in mitogen-supplemented soft agar, appear non-transformed in monolayer: they are well spread, nonrefractile, and contact inhibited. The existence of this new fibroblast phenotype demonstrates (a) that the growth factor and adhesion/TGF-beta 1 requirements for cell cycle progression are genetically separable, (b) that the two major control points in the fibroblast cell cycle (G0/G1 and G1/S) are regulated by distinct extracellular signals, and (c) that the genes regulating anchorage-independent growth need not be involved in regulating contact inhibition, focus formation, or growth factor dependence.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Anchorage-independent cell growth"

1

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.

Full text
Abstract:
In this thesis it is shown that PI 3-kinase is constitutively activated in SCLC cell lines (H69, H345 and H510). Inhibition of PI 3-kinase activity using the selective inhibitors wortmannin and LY294002 markedly inhibits cell proliferation and stimulates apoptosis in liquid media. This inhibition of proliferation is shown to occur via both ribosomal protein s6 kinase (p70s6kinase) dependent and independent mechanisms. Furthermore, PI 3-kinase inhibition reduced basal SCLC cell growth in agarose semi-solid media which could not be rescued by the addition of neuropeptides. This is the first description of a constitutively activated PI 3-kinase in any human cancer. It is proposed that this constitutive activity plays an important role in promoting growth, anchorage-independence and tumorigenicity in SCLC, and may account for the non-adherent phenotype and highly metastatic nature of this cancer. Resistance to chemotherapy is a major problem in the treatment of SCLC. Adhesion to extracellular matrix (ECM) proteins can protect cells from undergoing detachment-induced apoptosis. SCLC cells in vivo are surrounded by a specialized micro-environment rich in ECM containing in part laminin, fibronectin and collagen IV. It is shown that SCLC cells adhere to the ECM proteins in vitro in a β1 integrin-dependent manner, enhancing tumourigenicity and conferring resistance to standard chemotherapeutic agents. This adhesion to ECM proteins increases SCLC cell growth and protects cells from the pro-apoptotic effects of the chemotherapy agents via a β1-integrin-dependent mechanism requiring tyrosine kinase activation. Thus ECM proteins in vivo may provide a signal resulting in resistance to chemotherapy. These findings may begin to proivde us with novel targets for the therapeutic intervention of SCLC.
APA, Harvard, Vancouver, ISO, and other styles
2

Lawson, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Andrews, 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.

Full text
Abstract:
Integrins provide mechanical continuity between the extra- and intracellular environments. Upon binding to extracellular matrix (ECM), integrins interact with downstream effectors to promote cell adhesion, proliferation and migration. In contrast to its well-known role in adhesion, we have found that beta 1 integrin is also involved in the anchorage independent (AI) growth of prostate tumor cells. In concurrence with our previous findings, stable depletion of beta1 integrin in PC3 cells using an shRNA approach resulted in the complete inability of cells to form colonies in soft agarose, while adherent monolayer growth remained unaffected. In order to address the mechanism for beta1 integrin dependent AI growth, we examined the expression and localization of beta-catenin and E-cadherin, both of which are known to modulate AI growth. Migration and invasion through matrigel were found to be impeded by depletion of beta1 integrin. A qPCR array identified potential downstream targets that could be altered as a result of beta1 integrin depletion, these were further examined in all cell lines and it was found that TGFbeta1 is reduced in shITGB1 expressing cells. Taken together, these findings suggest a role for both beta1 integrin in driving anchorage independent growth and invasion of cancer cells.
APA, Harvard, Vancouver, ISO, and other styles
4

Saulnier, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Honeywell, 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.

Full text
Abstract:
Micro (mi)RNAs have recently been found to play an important role in cancer biology. In order to further understand how miRNAs affect prostate tumour progression, we evaluated miRNA expression in two invasive prostate tumour lines, PC3 and DU145. We then focused our evaluation on a novel miRNA, miR-105, whose levels were significantly decreased in both tumour cell lines as compared to normal prostate epithelial cells. As miR-105 levels were reduced in prostate tumour cell lines, we restored its expression following transfection of cells with mimic constructs to over-express miR-105 in both cell lines, in order to determine its effect on various tumourigenic properties. Over-expression caused decreased tumour cell proliferation, anchorage-independent growth and invasion in vitro and inhibited tumour growth in vivo. We further identified CDK6 as a putative target of miR-105, which likely contributed to its inhibition of tumour cell growth. Our results suggest that miR-105 inhibits tumour cell proliferation and may be an interesting target to regulate tumour growth or potentially used as a biomarker to differentiate between less and more aggressive tumours in patients.
APA, Harvard, Vancouver, ISO, and other styles
6

Shukla, 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.

Full text
Abstract:
Indiana University-Purdue University Indianapolis (IUPUI)
The 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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
Tumour metastasis remains the major cause of death in cancer patients and, to date, the mechanism and signalling pathways governing this process are not completely understood. The TGF-ß pathway is the most commonly mutated pathway in cancer, however its role in cancer progression is controversial as it can function as both a promoter and a suppressor of metastasis. Although previous studies have suggested a role for the molecular chaperone Hsp90 in regulating the TGF-ß pathway, the level at which this occurs as well as the consequences in terms of colon cancer metastasis are unknown.
APA, Harvard, Vancouver, ISO, and other styles
8

Wei-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.

Full text
Abstract:
碩士
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
碩士
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
碩士
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.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Anchorage-independent cell growth"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Goto, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

"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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Toole, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Centonze, 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.

Full text
Abstract:
Neuroblastoma, the most common extra-cranial pediatric solid tumor, is responsible for 9–15% of all pediatric cancer deaths. Its intrinsic heterogeneity makes it difficult to successfully treat, resulting in overall survival of 50% for half of the patients. Here we analyze the role in neuroblastoma of the adaptor protein p140Cap, encoded by the SRCIN1 gene. RNA-Seq profiles of a large cohort of neuroblastoma patients show that SRCIN1 mRNA levels are an independent risk factor inversely correlated to disease aggressiveness. In high-risk patients, SRCIN1 was frequently altered by hemizygous deletion, copy-neutral loss of heterozygosity, or disruption. Functional assays demonstrated that p140Cap is causal in dampening both Src and Jak2 kinase activation and STAT3 phosphorylation. Moreover, p140Cap expression decreases in vitro migration and anchorage-independent cell growth, and impairs in vivo tumor progression, in terms of tumor volume and number of spontaneous lung metastasis. p140Cap also contributes to an increased sensitivity of neuroblastoma cells to chemotherapy drugs and to the combined usage of doxorubicin and etoposide with Src inhibitors. Overall, we provide the first evidence that SRCIN1/p140Cap is a new independent prognostic marker for patient outcome and treatment, with a causal role in curbing the aggressiveness of neuroblastoma. We highlight the potential clinical impact of SRCIN1/p140Cap expression in neuroblastoma tumors, in terms of reducing cytotoxic effects of chemotherapy, one of the main issues for pediatric tumor treatment.
APA, Harvard, Vancouver, ISO, and other styles
6

Hamburger, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Anchorage-independent cell growth"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sato, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Jiang, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Guin, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Goydos, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Liao, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Goldenberg, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Wang, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

VanderVeen, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Rotem, 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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Anchorage-independent cell growth' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography