scholarly journals Role of mTOR Signaling in Tumor Cell Motility, Invasion and Metastasis

2016 ◽  
pp. 207-244
Keyword(s):  
Tumor Cell ◽  
Cell Motility ◽  
Mtor Signaling ◽  
Invasion And Metastasis ◽  
Tumor Cell Motility

scholarly journals The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors

2006 ◽  
Vol 173 (3) ◽  
pp. 395-404 ◽  
Author(s):  
Weigang Wang ◽  
Ghassan Mouneimne ◽  
Mazen Sidani ◽  
Jeffrey Wyckoff ◽  
Xiaoming Chen ◽  
...  
Keyword(s):  
Cell Motility ◽  
Cell Invasion ◽  
Actin Polymerization ◽  
Cancer Cell Invasion ◽  
Invasion And Metastasis ◽  
Over Expression ◽  
Cell Biol ◽  
Tumor Cell Motility ◽  
New Strategies

Understanding the mechanisms controlling cancer cell invasion and metastasis constitutes a fundamental step in setting new strategies for diagnosis, prognosis, and therapy of metastatic cancers. LIM kinase1 (LIMK1) is a member of a novel class of serine–threonine protein kinases. Cofilin, a LIMK1 substrate, is essential for the regulation of actin polymerization and depolymerization during cell migration. Previous studies have made opposite conclusions as to the role of LIMK1 in tumor cell motility and metastasis, claiming either an increase or decrease in cell motility and metastasis as a result of LIMK1 over expression (Zebda, N., O. Bernard, M. Bailly, S. Welti, D.S. Lawrence, and J.S. Condeelis. 2000. J. Cell Biol. 151:1119–1128; Davila, M., A.R. Frost, W.E. Grizzle, and R. Chakrabarti. 2003. J. Biol. Chem. 278:36868–36875; Yoshioka, K., V. Foletta, O. Bernard, and K. Itoh. 2003. Proc. Natl. Acad. Sci. USA. 100:7247–7252; Nishita, M., C. Tomizawa, M. Yamamoto, Y. Horita, K. Ohashi, and K. Mizuno. 2005. J. Cell Biol. 171:349–359). We resolve this paradox by showing that the effects of LIMK1 expression on migration, intravasation, and metastasis of cancer cells can be most simply explained by its regulation of the output of the cofilin pathway. LIMK1-mediated decreases or increases in the activity of the cofilin pathway are shown to cause proportional decreases or increases in motility, intravasation, and metastasis of tumor cells.

Abstract 3395: Role of ErbB3 signaling in tumor cell motility and metastasis

2010 ◽  
Author(s):  
Tatiana Smirnova ◽  
Jeffrey Wyckoff ◽  
Jeffrey E. Segall
Keyword(s):  
Tumor Cell ◽  
Cell Motility ◽  
Tumor Cell Motility ◽  
Erbb3 Signaling

scholarly journals Targeting tumor cell motility as a strategy against invasion and metastasis

2013 ◽  
Vol 34 (5) ◽  
pp. 283-289 ◽  
Author(s):  
Alan Wells ◽  
Jelena Grahovac ◽  
Sarah Wheeler ◽  
Bo Ma ◽  
Douglas Lauffenburger
Keyword(s):  
Tumor Cell ◽  
Cell Motility ◽  
Invasion And Metastasis ◽  
Tumor Cell Motility

scholarly journals The role of brevican in glioma: promoting tumor cell motility in vitro and in vivo

BMC Cancer ◽  
2012 ◽  
Vol 12 (1) ◽  
Author(s):  
Renquan Lu ◽  
Chengsheng Wu ◽  
Lin Guo ◽  
Yingchao Liu ◽  
Wei Mo ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Motility ◽  
Tumor Cell Motility

scholarly journals Understanding the Role of Elastic Modulus in the Relationship Between Second Harmonic Generation Scattering and Tumor Cell Motility

2020 ◽  
Author(s):  
Tresa M. Elias ◽  
Danielle E. Desa ◽  
Phong K. Nguyen ◽  
Ananya Goyal ◽  
Danielle Benoit ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Elastic Modulus ◽  
Tumor Cell ◽  
Cell Motility ◽  
Internal Structure ◽  
Collagen Fiber ◽  
Second Harmonic ◽  
Tumor Cell Motility ◽  
The Relationship

Abstract Background Second harmonic generation (SHG) is an intrinsic optical property of fibrillar collagen. SHG directionality is quantified by F/B, the ratio of forward- to backward-propagating signal, which is affected by collagen fiber internal structure, specifically the diameter, spacing, and disorder of fibrils within a collagen fiber. We have previously shown that F/B of primary invasive ductal carcinoma sections is prognostic of metastatic outcome. One possible cause of this relationship was revealed by our observation that tumor cells’ motility on collagen I gels varied when collagen fiber internal structure in those gels was manipulated. The mechanism by which tumor cells sense changes in collagen fiber internal structure remains unknown: here we evaluate the role of elastic modulus in the relationship between collagen fiber internal structure (as reported by F/B) and tumor cell motility. Methods The 4T1 murine mammary adenocarcinoma, a model of metastatic triple negative breast cancer, (TNBC) and the 67NR line, a non-metastatic luminal phenotype, were introduced to a series of collagen-polyacrylamide mixed gels wherein collagen fiber internal structure and gel elastic modulus were independently controlled. F/B was measured with SHG, while elastic modulus was measured globally via rheometry and locally via atomic force microscopy (AFM). Tumor cell motility was quantified over three hours. Results The motility of both cell lines varied with F/B while elastic modulus was held constant, and did so at two physiological modulus values. Interestingly, 4T1 cell motility increased as F/B increased, while 67NR cell motility decreased. Conclusions Our results suggest that elastic modulus does not play a significant role in the observed relationship between collagen fiber internal structure (as reported by F/B) and tumor cell motility, for two cell lines that are models of TNBC and luminal-like breast cancer. Our observation that the two lines exhibit opposite motility trends as F/B increases is consistent with the trends in metastatic outcome versus F/B observed in our published clinical data for luminal versus basal cohorts, and suggests that a tumor’s subtype may play a role in their response to collagen fiber internal structure.

scholarly journals Understanding the Role of Elastic Modulus in the Relationship Between Second Harmonic Generation Scattering and Tumor Cell Motility

2020 ◽  
Author(s):  
Tresa M. Elias ◽  
Danielle Desa ◽  
Phong Nguyen ◽  
Ananya Goyal ◽  
Danielle Benoit ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Elastic Modulus ◽  
Tumor Cell ◽  
Cell Motility ◽  
Internal Structure ◽  
Collagen Fiber ◽  
Second Harmonic ◽  
Tumor Cell Motility ◽  
The Relationship

Abstract Background: Second harmonic generation (SHG) is an intrinsic optical property of fibrillar collagen. SHG directionality is quantified by F/B, the ratio of forward- to backward-propagating signal, which is affected by collagen fiber internal structure, specifically the diameter, spacing, and disorder of fibrils within a collagen fiber. We have previously shown that F/B of primary invasive ductal carcinoma sections is prognostic of metastatic outcome. One possible cause of this relationship was revealed by our observation that tumor cells’ motility on collagen I gels varied when collagen fiber internal structure in those gels was manipulated. The mechanism by which tumor cells sense changes in collagen fiber internal structure remains unknown: here we evaluate the role of elastic modulus in the relationship between collagen fiber internal structure (as reported by F/B) and tumor cell motility. Methods: The 4T1 murine mammary adenocarcinoma, a model of metastatic triple negative breast cancer, (TNBC) and the 67NR line, a non-metastatic luminal phenotype, were introduced to a series of collagen-polyacrylamide mixed gels wherein collagen fiber internal structure and gel elastic modulus were independently controlled. F/B was measured with SHG, while elastic modulus was measured globally via rheometry and locally via atomic force microscopy (AFM). Tumor cell motility was quantified over three hours. Results: The motility of both cell lines varied with F/B while elastic modulus was held constant, and did so at two physiological modulus values. Interestingly, 4T1 cell motility increased as F/B increased, while 67NR cell motility decreased.Conclusions: Our results suggest that elastic modulus does not play a significant role in the observed relationship between collagen fiber internal structure (as reported by F/B) and tumor cell motility, for two cell lines that are models of TNBC and luminal-like breast cancer. Our observation that the two lines exhibit opposite motility trends as F/B increases is consistent with the trends in metastatic outcome versus F/B observed in our published clinical data for ER+ (i.e. containing the luminal subtypes) and ER- (i.e. containing the basal subtypes) cohorts, and suggests that a tumor’s subtype may play a role in their response to collagen fiber internal structure.

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