Journal articles: 'Anchorage-independent cell growth'

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Mori, S., J. T. Chang, E. R. Andrechek, N. Matsumura, T. Baba, G. Yao, J. W. Kim, M. Gatza, S. Murphy, and J. R. Nevins. "Anchorage-independent cell growth signature identifies tumors with metastatic potential." Oncogene 28, no. 31 (June 1, 2009): 2796–805. http://dx.doi.org/10.1038/onc.2009.139.

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Kuppumbatti, Yuvarani S., Brent Rexer, Shigeo Nakajo, Kazuyasu Nakaya, and Rafael Mira-y-Lopez. "CRBP suppresses breast cancer cell survival and anchorage-independent growth." Oncogene 20, no. 50 (November 2001): 7413–19. http://dx.doi.org/10.1038/sj.onc.1204749.

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Kang, J. S., and R. S. Krauss. "Ras induces anchorage-independent growth by subverting multiple adhesion-regulated cell cycle events." Molecular and Cellular Biology 16, no. 7 (July 1996): 3370–80. http://dx.doi.org/10.1128/mcb.16.7.3370.

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Anchorage-independent growth is a hallmark of transformed cells, but little is known of the molecular mechanisms that underlie this phenomenon. We describe here studies of cell cycle control of anchorage-independent growth induced by the ras oncogene, with the use of a somatic cell mutant fibroblast line (ER-1-2) that is specifically defective in oncogene-mediated, anchorage-independent growth. Control, nontransformed PKC3-F4 cells and ER-1-2 cells cannot proliferate in semisolid medium. Three important cell cycle events are dependent on adhesion of these cells to a substratum: phosphorylation of the retinoblastoma protein, pRB; cyclin E-dependent kinase activity; and cyclin A expression. PKC3-F4 cells that express ras (PKC3-F4/ras cells) proliferate in nonadherent cultures, and each of these three events occurs in the absence of adhesion in PKC3-F4/ras cells. Thus, ras can override the adhesion requirement of cellular functions that are necessary for cell cycle progression. ER-1-2 cells that express ras (ER-1-2/ras cells) possess hyperphosphorylated forms of pRB and cyclin E-dependent kinase activity in the absence of adhesion but remain adhesion dependent for expression of cyclin A. The adhesion dependence of pRB phosphorylation and cyclin E-dependent kinase activity is therefore dissociable from the adhesion dependence of cyclin A expression. Furthermore, ectopic expression of cyclin A is sufficient to rescue anchorage-independent growth of ER-1-2/ras cells but does not induce anchorage-independent growth of PKC3-F4 or ER-1-2 cells. However, like pRB phosphorylation and cyclin E-dependent kinase activity, the kinase activity associated with ectopically expressed cyclin A is dependent on cell adhesion, and this dependence is overcome by ras. Thus, the induction of anchorage-independent growth by ras may involve multiple signals that lead to both expression of cyclin A and activation of G1 cyclin-dependent kinase activities in the absence of cell adhesion.

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Liu, Heng-Jia, Lisa M. Ooms, Nuthasuda Srijakotre, Joey Man, Jessica Vieusseux, JoAnne E. Waters, Yue Feng, et al. "PtdIns(3,4,5)P3-dependent Rac Exchanger 1 (PREX1) Rac-Guanine Nucleotide Exchange Factor (GEF) Activity Promotes Breast Cancer Cell Proliferation and Tumor Growth via Activation of Extracellular Signal-regulated Kinase 1/2 (ERK1/2) Signaling." Journal of Biological Chemistry 291, no. 33 (June 29, 2016): 17258–70. http://dx.doi.org/10.1074/jbc.m116.743401.

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PtdIns(3,4,5)P3-dependent Rac exchanger 1 (PREX1) is a Rac-guanine nucleotide exchange factor (GEF) overexpressed in a significant proportion of human breast cancers that integrates signals from upstream ErbB2/3 and CXCR4 membrane surface receptors. However, the PREX1 domains that facilitate its oncogenic activity and downstream signaling are not completely understood. We identify that ERK1/2 MAPK acts downstream of PREX1 and contributes to PREX1-mediated anchorage-independent cell growth. PREX1 overexpression increased but its shRNA knockdown decreased ERK1/2 phosphorylation in response to EGF/IGF-1 stimulation, resulting in induction of the cell cycle regulators cyclin D1 and p21WAF1/CIP1. PREX1-mediated ERK1/2 phosphorylation, anchorage-independent cell growth, and cell migration were suppressed by inhibition of MEK1/2/ERK1/2 signaling. PREX1 overexpression reduced staurosporine-induced apoptosis whereas its shRNA knockdown promoted apoptosis in response to staurosporine or the anti-estrogen drug tamoxifen. Expression of wild-type but not GEF-inactive PREX1 increased anchorage-independent cell growth. In addition, mouse xenograft studies revealed that expression of wild-type but not GEF-dead PREX1 resulted in the formation of larger tumors that displayed increased phosphorylation of ERK1/2 but not AKT. The impaired anchorage-independent cell growth, apoptosis, and ERK1/2 signaling observed in stablePREX1knockdown cells was restored by expression of wild-type but not GEF-dead-PREX1. Therefore, PREX1-Rac-GEF activity is critical for PREX1-dependent anchorage-independent cell growth and xenograft tumor growth and may represent a possible therapeutic target for breast cancers that exhibit PREX1 overexpression.

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Telang, N. T., M. P. Osborne, L. A. Sweterlitsch, and R. Narayanan. "Neoplastic transformation of mouse mammary epithelial cells by deregulated myc expression." Cell Regulation 1, no. 11 (October 1990): 863–72. http://dx.doi.org/10.1091/mbc.1.11.863.

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A spontaneously immortalized, nontumorigenic mouse mammary epithelial cell line (MMEC) was transfected with an activated myc construct by electroporation. Constitutive expression of myc in MMEC resulted in anchorage independence in soft agar and tumorigenicity in nude mice. The myc-expressing MMEC showed higher saturation density, faster growth rate, and partial abrogation of serum-derived growth factor(s) requirement compared with parent MMEC. Epidermal growth factor or transforming growth factor alpha stimulated the anchorage-independent growth, but not the anchorage-dependent growth, of MMEC-myc cells. Type 1 transforming growth factor beta, on the other hand, inhibited both the anchorage-independent and anchorage-dependent growth of MMEC-myc cells. These results demonstrate that deregulated expression of myc results in neoplastic transformation iin mammary epithelial cells. Accompanying the transformation is altered sensitivity to polypeptide growth factors.

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Hervieu, Alexia, Sara Farrah Heuss, Chi Zhang, Rachel Barrow-McGee, Carine Joffre, Ludovic Ménard, Paul Andrew Clarke, and Stéphanie Kermorgant. "A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration." Science Signaling 13, no. 637 (June 23, 2020): eaba8627. http://dx.doi.org/10.1126/scisignal.aba8627.

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Receptor tyrosine kinases (RTKs) are often overexpressed or mutated in cancers and drive tumor growth and metastasis. In the current model of RTK signaling, including that of MET, downstream phosphatidylinositol 3-kinase (PI3K) mediates both cell proliferation and cell migration, whereas the small guanosine triphosphatase (GTPase) Rac1 mediates cell migration. However, in cultured NIH3T3 and glioblastoma cells, we found that class I PI3K mediated oncogenic MET–induced cell migration but not anchorage-independent growth. In contrast, Rac1 regulated both processes in distinct ways. Downstream of PI3K, Rac1 mediated cell migration through its GTPase activity, whereas independently of PI3K, Rac1 mediated anchorage-independent growth in a GTPase-independent manner through an adaptor function. Through its RKR motif, Rac1 formed a complex with the kinase mTOR to promote its translocation to the plasma membrane, where its activity promoted anchorage-independent growth of the cell cultures. Inhibiting mTOR with rapamycin suppressed the growth of subcutaneous MET-mutant cell grafts in mice, including that of MET inhibitor–resistant cells. These findings reveal a GTPase-independent role for Rac1 in mediating a PI3K-independent MET-to-mTOR pathway and suggest alternative or combined strategies that might overcome resistance to RTK inhibitors in patients with cancer.

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Uehara, Y., and N. Kitamura. "Expression of a human hepatocyte growth factor/scatter factor cDNA in MDCK epithelial cells influences cell morphology, motility, and anchorage-independent growth." Journal of Cell Biology 117, no. 4 (May 15, 1992): 889–94. http://dx.doi.org/10.1083/jcb.117.4.889.

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The addition of exogenous hepatocyte growth factor (HGF)/scatter factor (SF) to MDCK epithelial cells results in fibroblastic morphology and cell motility. We generated HGF/SF producing MDCK cells by transfection with an expression plasmid containing human HGF/SF cDNA. Production of HGF/SF by these cells induced a change from an epithelial to a fibroblastic morphology and increased cell motility. In addition, the HGF/SF producing cells acquired efficient anchorage-independent growth in soft agar but did not form tumors in nude mice. The morphological change and the stimulation of the anchorage-independent growth were prevented by anti-HGF/SF antibody, suggesting that the factor is secreted and then exerts its effects through cell surface receptors.

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Monami, Giada, Velia Emiliozzi, Alessandro Bitto, Francesca Lovat, Shi-Qiong Xu, Silvia Goldoni, Matteo Fassan, et al. "Proepithelin Regulates Prostate Cancer Cell Biology by Promoting Cell Growth, Migration, and Anchorage-Independent Growth." American Journal of Pathology 174, no. 3 (March 2009): 1037–47. http://dx.doi.org/10.2353/ajpath.2009.080735.

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McDermott, William G., Mathieu Boissan, Marie-Lise Lacombe, Patricia S. Steeg, and Christine E. Horak. "Nm23-H1 homologs suppress tumor cell motility and anchorage independent growth." Clinical & Experimental Metastasis 25, no. 2 (December 5, 2007): 131–38. http://dx.doi.org/10.1007/s10585-007-9128-0.

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Tavoloni, N., H. Inoue, H. Sabe, and H. Hanafusa. "v-src transformation of rat embryo fibroblasts. Inefficient conversion to anchorage-independent growth involves heterogeneity of primary cultures." Journal of Cell Biology 126, no. 2 (July 15, 1994): 475–83. http://dx.doi.org/10.1083/jcb.126.2.475.

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To clarify whether a single oncogene can transform primary cells in culture, we compared the transforming effect of a recombinant retrovirus (ZSV) containing the v-src gene in rat embryo fibroblasts (REFs) to that in the rat cell line 3Y1. In the focus assay, REFs exhibited resistance to transformation as only six foci were observed in the primary cultures as opposed to 98 in 3Y1 cells. After G418 selection, efficiency of transformation was again somewhat lower with REFs compared to that with 3Y1 cells, but the number of G418-resistant REF colonies was much greater than the number of foci in REF cultures. Furthermore, while 98% of G418-resistant colonies of ZSV-infected REFs were morphologically transformed, only 25% were converted to anchorage-independent growth, as opposed to 100% conversion seen in ZSV-infected 3Y1 cells. The poor susceptibility of REFs to anchorage-independent transformation did not involve differences in expression and subcellular distribution of p60v-src, or its kinase activity in vitro and in vivo. It rather reflected a property of the primary cultures, as cloning of REFs before ZSV infection demonstrated that only 2 out of 6 REF clones tested were permissive for anchorage-independent growth. The nonpermissive phenotype was dominant over the permissive one in somatic hybrid cells, and associated with organized actin filament bundles and a lower growth rate, both before and after ZSV infection. These results indicate that the poor susceptibility of REFs to anchorage-independent transformation by p60v-src reflects the heterogeneity of the primary cultures. REFs can be morphologically transformed by p60v-src with high efficiency but only a small fraction is convertible to anchorage-independent growth. REF resistance seems to involve the presence of a suppressor factor which may emerge from REF differentiation during embryonic development.

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Lee, Han Yeoung, Seung Wan Son, Sokviseth Moeng, Soo Young Choi, and Jong Kook Park. "The Role of Noncoding RNAs in the Regulation of Anoikis and Anchorage-Independent Growth in Cancer." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 627. http://dx.doi.org/10.3390/ijms22020627.

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Cancer is a global health concern, and the prognosis of patients with cancer is associated with metastasis. Multistep processes are involved in cancer metastasis. Accumulating evidence has shown that cancer cells acquire the capacity of anoikis resistance and anchorage-independent cell growth, which are critical prerequisite features of metastatic cancer cells. Multiple cellular factors and events, such as apoptosis, survival factors, cell cycle, EMT, stemness, autophagy, and integrins influence the anoikis resistance and anchorage-independent cell growth in cancer. Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are dysregulated in cancer. They regulate cellular signaling pathways and events, eventually contributing to cancer aggressiveness. This review presents the role of miRNAs and lncRNAs in modulating anoikis resistance and anchorage-independent cell growth. We also discuss the feasibility of ncRNA-based therapy and the natural features of ncRNAs that need to be contemplated for more beneficial therapeutic strategies against cancer.

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Lee, Han Yeoung, Seung Wan Son, Sokviseth Moeng, Soo Young Choi, and Jong Kook Park. "The Role of Noncoding RNAs in the Regulation of Anoikis and Anchorage-Independent Growth in Cancer." International Journal of Molecular Sciences 22, no. 2 (January 10, 2021): 627. http://dx.doi.org/10.3390/ijms22020627.

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Cancer is a global health concern, and the prognosis of patients with cancer is associated with metastasis. Multistep processes are involved in cancer metastasis. Accumulating evidence has shown that cancer cells acquire the capacity of anoikis resistance and anchorage-independent cell growth, which are critical prerequisite features of metastatic cancer cells. Multiple cellular factors and events, such as apoptosis, survival factors, cell cycle, EMT, stemness, autophagy, and integrins influence the anoikis resistance and anchorage-independent cell growth in cancer. Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), are dysregulated in cancer. They regulate cellular signaling pathways and events, eventually contributing to cancer aggressiveness. This review presents the role of miRNAs and lncRNAs in modulating anoikis resistance and anchorage-independent cell growth. We also discuss the feasibility of ncRNA-based therapy and the natural features of ncRNAs that need to be contemplated for more beneficial therapeutic strategies against cancer.

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Falsetti, Samuel C., De-an Wang, Hairuo Peng, Dora Carrico, Adrienne D. Cox, Channing J. Der, Andrew D. Hamilton, and Saïd M. Sebti. "Geranylgeranyltransferase I Inhibitors Target RalB To Inhibit Anchorage-Dependent Growth and Induce Apoptosis and RalA To Inhibit Anchorage-Independent Growth." Molecular and Cellular Biology 27, no. 22 (September 17, 2007): 8003–14. http://dx.doi.org/10.1128/mcb.00057-07.

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ABSTRACT Geranylgeranyltransferase I inhibitors (GGTIs) are presently undergoing advanced preclinical studies and have been shown to disrupt oncogenic and tumor survival pathways, to inhibit anchorage-dependent and -independent growth, and to induce apoptosis. However, the geranylgeranylated proteins that are targeted by GGTIs to induce these effects are not known. Here we provide evidence that the Ras-like small GTPases RalA and RalB are exclusively geranylgeranylated and that inhibition of their geranylgeranylation mediates, at least in part, the effects of GGTIs on anchorage-dependent and -independent growth and tumor apoptosis. To this end, we have created the corresponding carboxyl-terminal mutants that are exclusively farnesylated and verified that they retain the subcellular localization and signaling activities of the wild-type geranylgeranylated proteins and that Ral GTPases do not undergo alternative prenylation in response to GGTI treatment. By expressing farnesylated, GGTI-resistant RalA and RalB in Cos7 cells and human pancreatic MiaPaCa2 cancer cells followed by GGTI-2417 treatment, we demonstrated that farnesylated RalB, but not RalA, confers resistance to the proapoptotic and anti-anchorage-dependent growth effects of GGTI-2417. Conversely, farnesylated RalA but not RalB expression renders MiaPaCa2 cells less sensitive to inhibition of anchorage-independent growth. Furthermore, farnesylated RalB, but not RalA, inhibits the ability of GGTI-2417 to suppress survivin and induce p27 Kip1 protein levels. We conclude that RalA and RalB are important, functionally distinct targets for GGTI-mediated tumor apoptosis and growth inhibition.

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Lee, Sophia Boyoung, Kai Doberstein, Peter Baumgarten, Anja Wieland, Christopher Ungerer, Claudia Bürger, Katja Hardt, et al. "PAX2 Regulates ADAM10 Expression and Mediates Anchorage-Independent Cell Growth of Melanoma Cells." PLoS ONE 6, no. 8 (August 18, 2011): e22312. http://dx.doi.org/10.1371/journal.pone.0022312.

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Reiter, T., S. Penman, and D. G. Capco. "Shape-dependent regulation of cytoskeletal protein synthesis in anchorage-dependent and anchorage-independent cells." Journal of Cell Science 76, no. 1 (June 1, 1985): 17–33. http://dx.doi.org/10.1242/jcs.76.1.17.

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We examine changes in protein synthesis that accompany suspension (i.e. shape alteration) of anchorage-dependent and anchorage-independent cells using a newly developed cell fractionation procedure based on detergent extraction. Using this procedure, a cell can be divided into four distinct and independent fractions: soluble, cytoskeleton, chromatin and nuclear matrix-intermediate filament. This fractionation procedure is used to investigate protein synthetic events associated with the release from anchorage-dependent growth, characteristic of transformed cells. Suspension results in several unexpected events in both anchorage-dependent (3T3) cells and anchorage-independent (SVPy 3T3) cells. Suspension of 3T3 cells results in a reduction of total protein synthesis; however, two proteins are enhanced in their amount of synthesis. Suspension of SVPy 3T3 results in about 20 proteins proceeding through short and long-term alterations in the rate of synthesis. The synthesis of some of these proteins is inhibited, others undergo a transient decrease in synthesis upon suspension and then increase above their rate in the anchored state, while the synthesis of others steadily increases after suspension. Suspension of anchorage-dependent cells results in a fraction specific shift in the rates of protein synthesis. Possible roles for these fraction-specific proteins are considered.

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Li, Xiao-Su, Zhi-Ming Shao, M. Saeed Sheikh, Julie L. Eiseman, Dorothy Sentz, Anton M. Jetten, Jian-Chyi Chen, et al. "Retinoic acid nuclear receptor ? inhibits breast carcinoma anchorage independent growth." Journal of Cellular Physiology 165, no. 3 (December 1995): 449–58. http://dx.doi.org/10.1002/jcp.1041650302.

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Saulnier, Ron, Bhavna Bhardwaj, Jennifer Klassen, Doris Leopold, Nader Rahimi, Eric Tremblay, Deane Mosher, and Bruce Elliott. "Fibronectin Fibrils and Growth Factors Stimulate Anchorage-Independent Growth of a Murine Mammary Carcinoma." Experimental Cell Research 222, no. 2 (February 1996): 360–69. http://dx.doi.org/10.1006/excr.1996.0045.

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28

Rintoul, Robert C., Robert C. Buttery, Alison C. Mackinnon, Weng Sie Wong, Deane Mosher, Christopher Haslett, and Tariq Sethi. "Cross-Linking CD98 Promotes Integrin-like Signaling and Anchorage-independent Growth." Molecular Biology of the Cell 13, no. 8 (August 2002): 2841–52. http://dx.doi.org/10.1091/mbc.01-11-0530.

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CD98, an early marker of T-cell activation, is an important regulator of integrin-mediated adhesion events. Previous studies suggest that CD98 is coupled to both cellular activation and transformation and is involved in the pathogenesis of viral infection, inflammatory disease, and cancer. Understanding of the molecular mechanisms underlying CD98 activity may have far-reaching practical applications in the development of novel therapeutic strategies in these disease states. Using small cell lung cancer cell lines, which are nonadherent, nonpolarized, and highly express CD98, we show that, in vitro, under physiological conditions, CD98 is constitutively associated with β1 integrins regardless of activation status. Cross-linking CD98 with the monoclonal antibody 4F2 stimulated phosphatidylinositol (PI) 3-kinase, PI(3,4,5)P3, and protein kinase B in the absence of integrin ligation or extracellular matrix engagement. Furthermore, cross-linking CD98 promoted anchorage-independent growth. Using fibroblasts derived from β1 integrin null stem cells (GD25), wild-type GD25β1, or GD25 cells expressing a mutation preventing β1 integrin-dependent FAK phosphorylation, we demonstrate that a functional β1 integrin is required for CD98 signaling. We propose that by cross-linking CD98, it acts as a “molecular facilitator” in the plasma membrane, clustering β1 integrins to form high-density complexes. This results in integrin activation, integrin-like signaling, and anchorage-independent growth. Activation of PI 3-kinase may, in part, explain cellular transformation seen on overexpressing CD98. These results may provide a paradigm for events involved in such diverse processes as inflammation and viral-induced cell fusion.

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Yamazaki, Yuji, Yoshito Kaziro, and Hiroshi Koide. "Ral Promotes Anchorage-Independent Growth of a Human Fibrosarcoma, HT10801." Biochemical and Biophysical Research Communications 280, no. 3 (January 2001): 868–73. http://dx.doi.org/10.1006/bbrc.2000.4233.

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30

Sanfilippo, Brunella, Fortunato Ciardiello, David S. Salomon, and William R. Kidwell. "Growth of cells on a perfluorocarbon-medium interphase: A quantitative assay for anchorage-independent cell growth." In Vitro Cellular & Developmental Biology 24, no. 1 (January 1988): 71–78. http://dx.doi.org/10.1007/bf02623818.

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31

Hara, Yoshinori. "ANALYSIS OF ANCHORAGE INDEPENDENT GROWTH OF HUMAN PROSTATE CANCER CELL LINE LNCAP." Japanese Journal of Urology 83, no. 9 (1992): 1429–35. http://dx.doi.org/10.5980/jpnjurol1989.83.1429.

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Higgins, T. E., A. C. Murphy, J. M. Staddon, A. J. Lax, and E. Rozengurt. "Pasteurella multocida toxin is a potent inducer of anchorage-independent cell growth." Proceedings of the National Academy of Sciences 89, no. 10 (May 15, 1992): 4240–44. http://dx.doi.org/10.1073/pnas.89.10.4240.

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33

Zhou, Donghui, Maya Z. Springer, David Xu, Degang Liu, Andy Hudmon, Kay F. Macleod, and Samy O. Meroueh. "Small molecules inhibit STAT3 activation, autophagy, and cancer cell anchorage-independent growth." Bioorganic & Medicinal Chemistry 25, no. 12 (June 2017): 2995–3005. http://dx.doi.org/10.1016/j.bmc.2017.03.048.

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Kanatsu-Shinohara, Mito, Kimiko Inoue, Jiyoung Lee, Hiromi Miki, Narumi Ogonuki, Shinya Toyokuni, Atsuo Ogura, and Takashi Shinohara. "Anchorage-Independent Growth of Mouse Male Germline Stem Cells In Vitro1." Biology of Reproduction 74, no. 3 (March 1, 2006): 522–29. http://dx.doi.org/10.1095/biolreprod.105.046441.

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Liu, Xuesong, Yan Shi, Edward K. H. Han, Zehan Chen, Saul H. Rosenberg, Vincent L. Giranda, Yan Luo, and Shi-Chung Ng. "Downregulation of Akt1 Inhibits Anchorage-Independent Cell Growth and Induces Apoptosis in Cancer Cells." Neoplasia 3, no. 4 (2001): 278–86. http://dx.doi.org/10.1038/sj.neo.7900163.

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Kantak, Seema S., and Randall H. Kramer. "E-cadherin Regulates Anchorage-independent Growth and Survival in Oral Squamous Cell Carcinoma Cells." Journal of Biological Chemistry 273, no. 27 (July 3, 1998): 16953–61. http://dx.doi.org/10.1074/jbc.273.27.16953.

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Wu, Feng, Ashley Jordan, Thomas Kluz, Steven Shen, Hong Sun, Laura A. Cartularo, and Max Costa. "SATB2 expression increased anchorage-independent growth and cell migration in human bronchial epithelial cells." Toxicology and Applied Pharmacology 293 (February 2016): 30–36. http://dx.doi.org/10.1016/j.taap.2016.01.008.

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Cerezo, Ana, Marta C. Guadamillas, Jacky G. Goetz, Sara Sánchez-Perales, Eric Klein, Richard K. Assoian, and Miguel A. del Pozo. "The Absence of Caveolin-1 Increases Proliferation and Anchorage- Independent Growth by a Rac-Dependent, Erk-Independent Mechanism." Molecular and Cellular Biology 29, no. 18 (July 20, 2009): 5046–59. http://dx.doi.org/10.1128/mcb.00315-09.

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ABSTRACT Anchorage-independent growth (AIG) of cancer cells requires escape from integrin-mediated signals. A protein frequently downregulated in cancer, caveolin-1 (Cav1), mediates integrin control of several growth-regulatory pathways. We report that loss of Cav1 results in faster exit from quiescence and progress through the cell cycle, proliferation without anchorage to substrate, and absence of cyclin D1 downregulation upon serum deprivation or detachment. Surprisingly, this proliferative advantage is independent of Erk-mitogen-activated protein kinase signaling; instead, cyclin expression and cell cycle progression in the absence of Cav1 are driven by increased membrane order and Rac targeting. AIG was induced in Cav1-expressing cells by forced membrane targeting of Rac1 or by inhibiting Cav1-mediated internalization of plasma membrane ordered domains at which Rac1 accumulates. Restoring Rho activity, which is downregulated after loss of Cav1, antagonizes Rac1 and prevents cyclin D1 accumulation after serum starvation or loss of adhesion. Anchorage independence and increased proliferation in Cav1-deficient tumoral and null cells are thus due to an increased fraction of active Rac1 at membrane ordered domains. These results provide insight into the mechanisms regulating growth of cancer cells, which frequently lose Cav1 function.

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39

Renshaw, Mark W., Leo S. Price, and Martin Alexander Schwartz. "Focal Adhesion Kinase Mediates the Integrin Signaling Requirement for Growth Factor Activation of Map Kinase." Journal of Cell Biology 147, no. 3 (November 1, 1999): 611–18. http://dx.doi.org/10.1083/jcb.147.3.611.

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The mitogen-activated protein (MAP) kinase pathway is a critical regulator of cell growth, migration, and differentiation. Growth factor activation of MAP kinase in NIH 3T3 cells is strongly dependent upon integrin-mediated adhesion, an effect that contributes to the anchorage dependence of normal cell growth. We now show that expression of constructs that constitutively activate focal adhesion kinase (FAK) rescued the defect in serum activation of MAP kinase in suspended cells without directly activating MAP kinase. Dominant negative FAK blocked both the rescue of suspended cells by the activated construct and the serum activation of MAP kinase in adherent cells. MAP kinase in FAK−/− mouse embryo fibroblasts was adhesion-insensitive, and reexpression of FAK restored its adhesion dependence. MAP kinase activity in ras-transformed cells is still decreased in suspension, but expression of constructs that constitutively activate FAK enhanced their anchorage-independent growth without increasing adherent growth. V-src, which activates both Ras and FAK, induced MAP kinase activation that was insensitive to loss of adhesion, and that was blocked by a dominant negative FAK. These results demonstrate that FAK mediates the integrin requirement for serum activation of MAP kinase in normal cells, and that bypassing this mechanism contributes to anchorage-independent growth in transformed cells.

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40

Pandey, Vijay, Jo K. Perry, Kumarasamypet M. Mohankumar, Xiang-Jun Kong, Shu-Min Liu, Zheng-Sheng Wu, Murray D. Mitchell, Tao Zhu, and Peter E. Lobie. "Autocrine Human Growth Hormone Stimulates Oncogenicity of Endometrial Carcinoma Cells." Endocrinology 149, no. 8 (May 1, 2008): 3909–19. http://dx.doi.org/10.1210/en.2008-0286.

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Recent published data have demonstrated elevated levels of human GH (hGH) in endometriosis and endometrial adenocarcinoma. Herein, we demonstrate that autocrine production of hGH can enhance the in vitro and in vivo oncogenic potential of endometrial carcinoma cells. Forced expression of hGH in endometrial carcinoma cell lines RL95-2 and AN3 resulted in an increased total cell number through enhanced cell cycle progression and decreased apoptotic cell death. In addition, autocrine hGH expression in endometrial carcinoma cells promoted anchorage-independent growth and increased cell migration/invasion in vitro. In a xenograft model of human endometrial carcinoma, autocrine hGH enhanced tumor size and progression. Changes in endometrial carcinoma cell gene expression stimulated by autocrine hGH was consistent with the altered in vitro and in vivo behavior. Functional antagonism of hGH in wild-type RL95-2 cells significantly reduced cell proliferation, cell survival, and anchorage-independent cell growth. These studies demonstrate a functional role for autocrine hGH in the development and progression of endometrial carcinoma and indicate potential therapeutic relevance of hGH antagonism in the treatment of endometrial carcinoma.

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Qiu, R. G., A. Abo, F. McCormick, and M. Symons. "Cdc42 regulates anchorage-independent growth and is necessary for Ras transformation." Molecular and Cellular Biology 17, no. 6 (June 1997): 3449–58. http://dx.doi.org/10.1128/mcb.17.6.3449.

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The Rho family members Cdc42, Rac, and Rho play a central role in the organization of the actin cytoskeleton and regulate transcription. Whereas Rac and Rho have been implicated in transformation by oncogenic Ras, the role of Cdc42 in this process remains unknown. In this study, we found that Rat1 fibroblasts expressing constitutively active V12-Cdc42 were anchorage independent and proliferated in nude mice but failed to show enhanced growth in low serum. Similar to V12-Rac1-expressing Rat1 fibroblasts, V12-Cdc42 lines displayed a high frequency of multinucleated cells. Interestingly, coexpression of dominant negative N17-Rac1 blocked the V12-Cdc42-induced multinucleated phenotype but not growth in soft agar, indicating that Cdc42 controls anchorage independence in a Rac-independent fashion. We also showed that dominant negative N17-Cdc42 inhibited Ras focus formation and anchorage-independent growth and caused reversion of the transformed morphology, indicating that Cdc42 is necessary for Ras transformation. N17-Cdc42 caused only partial inhibition of Ras-induced low-serum growth, however. In contrast, whereas N17-Rac1 also effectively inhibited Ras-induced anchorage independence, it did not revert the morphology of Ras-transformed cells. N17-Rac1 strongly inhibited low-serum growth of Ras-transformed cells, however. Together, these data provide a novel function for Cdc42 in cell proliferation and indicate that Cdc42 and Rac play distinct roles in growth control and Ras transformation.

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42

Rivera, R. T., S. G. Pasion, D. T. Wong, Y. B. Fei, and D. K. Biswas. "Loss of tumorigenic potential by human lung tumor cells in the presence of antisense RNA specific to the ectopically synthesized alpha subunit of human chorionic gonadotropin." Journal of Cell Biology 108, no. 6 (June 1, 1989): 2423–34. http://dx.doi.org/10.1083/jcb.108.6.2423.

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A clonal strain of human lung tumor cells in culture (ChaGo), derived from a bronchogenic carcinoma, synthesizes and secretes large amounts of alpha (alpha) and a comparatively lower level of beta (beta) subunit of the glycoprotein hormone, human chorionic gonadotropin (HCG). ChaGo cells lost their characteristic anchorage-independent growth phenotype in the presence of anti-alpha-HCG antibody. The effect of the antibody was partially reversed by addition of alpha-HCG to the culture medium. ChaGo cells were transfected with an expression vector (pRSV-anti-alpha-HCG), that directs synthesis of RNA complementary to alpha-HCG mRNA. The transfectants produced alpha-HCG antisense RNA which was associated with the reduced level of alpha-HCG. Transfectants also displayed several altered phenotypic properties, including altered morphology, less mitosis, reduced growth rate, loss of anchorage-independent growth, and loss of tumorigenicity in nude mice. Treatment of transfectants with 8,bromo-cAMP resulted in increased accumulation of alpha-HCG mRNA, no change in the level of alpha-HCG antisense RNA, release of the inhibition of [3H]thymidine incorporation, and restoration of anchorage-independent growth phenotype. The overexpression of c-myc, observed in ChaGo cells, was unaffected by the reduced level of alpha-HCG. These results suggest that ectopic synthesis of the alpha subunit of HCG plays a functional role in the transformation of these human lung cells.

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Murphy, P. R. "Phosphorothioate antisense oligonucleotides against basic fibroblast growth factor inhibit anchorage-dependent and anchorage-independent growth of a malignant glioblastoma cell line." Molecular Endocrinology 6, no. 6 (June 1, 1992): 877–84. http://dx.doi.org/10.1210/me.6.6.877.

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44

Murphy, P. R., Y. Sato, and R. S. Knee. "Phosphorothioate antisense oligonucleotides against basic fibroblast growth factor inhibit anchorage-dependent and anchorage-independent growth of a malignant glioblastoma cell line." Molecular Endocrinology 6, no. 6 (June 1992): 877–84. http://dx.doi.org/10.1210/mend.6.6.1323055.

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45

Watanabe, Masashi, Tadasuke Tsukiyama, and Shigetsugu Hatakeyama. "TRIM31 interacts with p52Shc and inhibits Src-induced anchorage-independent growth." Biochemical and Biophysical Research Communications 388, no. 2 (October 2009): 422–27. http://dx.doi.org/10.1016/j.bbrc.2009.08.028.

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46

Shibanuma, Motoko, Kazunori Mori, and Kiyoshi Nose. "HIC-5: A Mobile Molecular Scaffold Regulating the Anchorage Dependence of Cell Growth." International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/426138.

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HIC-5 is a multidomain LIM protein homologous to paxillin that serves as a molecular scaffold at focal adhesions and in the nucleus. It forms mobile molecular units with LIM-only proteins, PINCH, and CRP2 and translocates in and out of the nucleus via a nuclear export signal (NES). Of note, NES of HIC-5 is distinctive in its sensitivity to the cellular redox state. Recently, the mobile units of HIC-5 have been suggested to be involved in the regulation of the anchorage dependence of cell growth. On loss of adhesion, an increase in reactive oxygen species in the cells modifies NES and stops shuttling, which leads to cell-cycle control. More specifically, the system circumvents nuclear localization of cyclin D1 and transactivatesp21Cip1in detached cells, thereby avoiding anchorage-independent cell growth. Thus, the HIC-5-LIM only protein complex has emerged as a fail-safe system for regulating the anchorage dependence of cell growth.

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Harding, Paul A., Karen M. Davis-Fleischer, Melissa A. Crissman-Combs, Matthew T. Miller, David R. Brigstock, and Gail E. Besner. "Induction of Anchorage Independent Growth by Heparin-binding EGF-like Growth Factor (HB-EGF)." Growth Factors 17, no. 1 (January 1999): 49–61. http://dx.doi.org/10.3109/08977199909001062.

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48

Bush, Jason A., and Gang Li. "Anchorage-Independent Growth of p53-Knockout Dermal Fibroblasts is Reversed by Wild-Type p53." Journal of Cutaneous Medicine and Surgery 5, no. 1 (January 2001): 18–24. http://dx.doi.org/10.1177/120347540100500105.

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Background: p53 is a 393-residue nuclear phosphoprotein. Mutation of p53 occurs in over half of all human cancers and thus is a crucial step in the process of cell transformation and tumorigenesis. Since tumorigenesis is a multistep process, it generally requires the mutation of certain key oncogenes and/or tumor-suppressor genes. Using p53-deficient mice, we can investigate the p53-dependent mechanisms leading to tumorigenesis. Objective: To examine the unique anchorage-independent growth characteristics of dermal fibroblasts isolated from p53-deficient mice. Methods: The growth characteristics of highly confluent cultured dermal fibroblasts from wild-type ( p53+/+) and p53-deficient ( p53−/−) mice were compared by DNA fragmentation assay, colony formation in soft agar, and overexpression of a wild-type p53 transgene in p53-deficient cells. Results: p53−/− fibroblasts have a growth rate dramatically higher than p53+/+ cells and detach from plastic cultureware at high density. The detachment of p53−/− cells is not due to apoptosis. Furthermore, these cells have the capacity to grow in soft agar—a hallmark of cell transformation—and this anchorage-independent growth can be reversed by the introduction of a wild-type p53 transgene. Conclusion: Dermal fibroblasts isolated from p53-deficient mice show anchorage-independent growth. Therefore, the absence of p53 is sufficient for the initiation of cell transformation in this cell type and establishes this model system as an excellent tool to dissect the molecular steps involved in oncogenesis.

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Palmer, Helen J., Veronica M. Maher, and J. Justin Mc Cormick. "Effect of retinoids on growth factor-induced anchorage independent growth of human fibroblasts." In Vitro Cellular & Developmental Biology 25, no. 11 (November 1989): 1009–15. http://dx.doi.org/10.1007/bf02624134.

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Palmer, Helen, Veronica M. Maher, and J. Justin McCormick. "Platelet-derived growth factor or basic fibroblast growth factor induce anchorage-independent growth of human fibroblasts." Journal of Cellular Physiology 137, no. 3 (December 1988): 588–92. http://dx.doi.org/10.1002/jcp.1041370328.

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

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