scholarly journals Hyperphosphorylated FAK Delocalizes from Focal Adhesions to Membrane Ruffles

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Abdelkader Hamadi ◽  
Therese B. Deramaudt ◽  
Kenneth Takeda ◽  
Philippe Rondé
Keyword(s):  
Tumor Metastasis ◽  
Focal Adhesions ◽  
Downstream Signaling ◽  
Astrocytoma Cells ◽  
Src Inhibitor ◽  
Human Astrocytoma ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Downstream Signaling Pathway ◽  
Human Astrocytoma Cells

Cell adhesion and migration are key determinants in tumor metastasis. Adherence of tumor cell to the extracellular matrix is mediated via integrin containing focal adhesions (FAs). Binding of integrins to ECM triggers phosphorylation of two major components of FAs, focal adhesion kinase (FAK) and Src, activating downstream signaling pathway which leads to FA disassembly and cell migration. In this paper, we analyze how phosphorylation of FAK regulates its trafficking at FAs in living human astrocytoma cells. Upon pervanadate-induced FAK phosphorylation, phosphorylated FAK appeared highly expressed at newly formed membrane ruffles. This effect was abolished in presence of the specific Src inhibitor PP2. Our findings demonstrate that upon phosphorylation, FAK delocalizes from FAs to membrane ruffles.

scholarly journals Progesterone Induces the Growth and Infiltration of Human Astrocytoma Cells Implanted in the Cerebral Cortex of the Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Liliana Germán-Castelán ◽  
Joaquín Manjarrez-Marmolejo ◽  
Aliesha González-Arenas ◽  
María Genoveva González-Morán ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Motor Cortex ◽  
Male Rats ◽  
Astrocytoma Cells ◽  
Intracellular Receptor ◽  
Human Astrocytoma ◽  
And Migration ◽  
Astrocytoma Grade Iii ◽  
Antagonist Ru486 ◽  
U373 Cells ◽  
Human Astrocytoma Cells

Progesterone (P4) promotes cell proliferation in several types of cancer, including brain tumors such as astrocytomas, the most common and aggressive primary intracerebral neoplasm in humans. In this work, we studied the effects of P4and its intracellular receptor antagonist, RU486, on growth and infiltration of U373 cells derived from a human astrocytoma grade III, implanted in the motor cortex of adult male rats, using two treatment schemes. In the first one, fifteen days after cells implantation, rats were daily subcutaneously treated with vehicle (propylene glycol, 160 μL), P4(1 mg), RU486 (5 mg), or P4+ RU486 (1 mg and 5 mg, resp.) for 21 days. In the second one, treatments started 8 weeks after cells implantation and lasted for 14 days. In both schemes we found that P4significantly increased the tumor area as compared with the rest of the treatments, whereas RU486 blocked P4effects. All rats treated with P4showed tumor infiltration, while 28.6% and 42.9% of the animals treated with RU486 and P4+ RU486, respectively, presented it. Our data suggest that P4promotes growth and migration of human astrocytoma cells implanted in the motor cortex of the rat through the interaction with its intracellular receptor.

Specific attachment and migration of human astrocytoma cells on human but not murine laminin

Glia ◽  
1995 ◽  
Vol 13 (1) ◽  
pp. 64-74 ◽  
Author(s):  
Alf Giese ◽  
Monique D. Rief ◽  
Nhan L. Tran ◽  
Michael E. Berens
Keyword(s):  
Astrocytoma Cells ◽  
Specific Attachment ◽  
Human Astrocytoma ◽  
And Migration ◽  
Human Astrocytoma Cells

Progesterone promotes cell migration, invasion and cofilin activation in human astrocytoma cells

Steroids ◽  
2016 ◽  
Vol 105 ◽  
pp. 19-25 ◽  
Author(s):  
Ana Gabriela Piña-Medina ◽  
Valeria Hansberg-Pastor ◽  
Aliesha González-Arenas ◽  
Marco Cerbón ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Cell Migration ◽  
Astrocytoma Cells ◽  
Human Astrocytoma ◽  
Human Astrocytoma Cells

Inhibition of lactate-induced swelling by dichloroacetate in human astrocytoma cells

1991 ◽  
Vol 568 (1-2) ◽  
pp. 92-100 ◽  
Author(s):  
Jose L. Tomsig ◽  
Eric Gruenstein ◽  
Ruth V.W. Dimlich
Keyword(s):  
Astrocytoma Cells ◽  
Human Astrocytoma ◽  
Human Astrocytoma Cells

CIP4 Targeted to Recruit GTP-Cdc42 Involving in Invadopodia Formation Through NF-κB Signaling Pathway Promotes Invasion and Metastasis of Colorectal Cancer

2021 ◽  
Author(s):  
Zhiyan Hu ◽  
Jiaxian Zhu ◽  
Yidan Ma ◽  
Ting Long ◽  
Lingfang Gao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Tumor Metastasis ◽  
Migration And Invasion ◽  
Downstream Signaling ◽  
And Function ◽  
Downstream Signaling Pathway ◽  
Invadopodia Formation

Abstract Background CIP4 (Cdc42-interacting protein 4), a member of the F-BAR family which plays an important role in regulating cell membrane and actin, has been reported to interact with Cdc42 and closely associated with tumor invadopodia formation. However, the specific mechanism of the interaction between CIP4 and Cdc42 as well as the downstream signaling pathway in response in colorectal cancer (CRC) remains unknown, which is worth exploring for its impact on tumor infiltration and metastasis. Methods Immunohistochemistry and western blot analyses were performed to detect the expression of CIP4 and Cdc42. Their relationship with CRC clinicopathological characteristics was further analyzed. Wound-healing, transwell migration and invasion assays tested the effect of CIP4 on cells migration and invasion ability in vitro, and the orthotopic xenograft colorectal cancer mouse mode evaluated the tumor metastasis in vivo. The invadopodia formation and function were assessed by immunofluorescence, scanning electron microscopy (SEM) and matrix degradation assay. The interaction between CIP4 and Cdc42 was confirmed by co-immunoprecipitation (co-IP) and GST-Pull down assays. Immunofluorescence was used to observed the colocalization of CIP4, GTP-Cdc42 and invadopodia. The related downstream signaling pathway was investigated by western blot and immunofluorescence. Results CIP4 expression was significantly higher in human colorectal cancer tissues and correlated with the CRC infiltrating depth and metastasis as well as the lower survival rate in patients. In cultured CRC cells, knockdown of CIP4 inhibited cell migration and invasion ability in vitro and the tumor metastasis in vivo, while overexpression of CIP4 confirmed the opposite situation by promoting invadopodia formation and matrix degradation ability. In addition, we identified GTP-Cdc42 as a directly interactive protein of CIP4, which was upregulated and recruited by CIP4 to participate in this process. Furthermore, activated NF-κB signaling pathway was found in CIP4 overexpression CRC cells contributing to invadopodia formation while inhibition of either CIP4 or Cdc42 led to suppression of NF-κB pathway resulted in decrease quantity of invadopodia. Conclusion Our findings suggested that CIP4 targets to recruit GTP-Cdc42 and directly combines with it to accelerate invadopodia formation and function by activating NF-κB signaling pathway, thus promoting CRC infiltration and metastasis.

Sign in / Sign up

Export Citation Format

Share Document