Expression of complete keratin filaments in mouse L cells augments cell migration and invasion.

Chu, Yi; Runyan, Raymond B.; Oshima, Robert G.; Hendrix, Mary J.C.

doi:10.1073/pnas.90.9.4261

Cited by 146 publications

(121 citation statements)

References 29 publications

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“…In all, 24-well plates with precoated growth factor reduced Matrigel (Matrigel-GFR) chambers (BD Biosciences) were prepared according to the manufacturer's instructions (Albini et al, 1987;Chu et al, 1993). The lower well of the chamber was filled with DMEM þ 0.1% BSA.…”

Section: Matrigelt-gfr Invasion Assaymentioning

confidence: 99%

Erythropoietin-mediated activation of JAK-STAT signaling contributes to cellular invasion in head and neck squamous cell carcinoma

et al. 2005

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Originally characterized as a growth factor for erythrocytes, erythropoietin (EPO) is used to treat anemia and fatigue in cancer patients receiving radiation therapy and chemotherapy. EPO and the EPO receptor (EPOR) are expressed in nonhematopoietic cells and cancers. However, the role of EPO and EPOR within nonhematopoietic cancer cells remains incompletely understood. Although a recent clinical trial demonstrated worse tumor control and survival in head and neck cancer patients treated with EPO, the role of EPO and EPOR in head and neck squamous cell carcinoma (HNSCC) has not been examined. In the present study, we demonstrate the previously unrecognized EPO-mediated invasion by HNSCC cells through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway. Furthermore, we confirmed the expression of EPO and EPOR in a panel of human HNSCC cell lines and tissue specimens. Pharmacological doses of EPO also had a limited proliferation effect in these cell lines. These results define a novel role for EPO in mediating tumor cell invasion. Increased levels of EPO and EPOR in lymph node metastases as compared to primary tumors from HNSCC patients further support the role of EPO/EPOR in HNSCC disease progression and metastasis.

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Section: Matrigelt-gfr Invasion Assaymentioning

confidence: 99%

Erythropoietin-mediated activation of JAK-STAT signaling contributes to cellular invasion in head and neck squamous cell carcinoma

et al. 2005

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“…We further examined the in vitro invasion ability of NIH3T3 cells stably expressing EGFR mutants compared with those expressing WT EGFR by BD Matrigel invasion assays (Chu et al, 1993;Sato et al, 1994). NIH3T3 is a noninvasive cell line (Sato et al, 1994).…”

Section: Enhanced Invasion By Egfr Mutantsmentioning

confidence: 99%

Epidermal growth factor receptor activation in prostate cancer by three novel missense mutations

et al. 2008

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While epidermal growth factor receptor (EGFR) dysregulation is known to play a critical role in prostate carcinogenesis, there has been no direct evidence indicating EGFR mutations induce tumorigenesis in prostate cancer. We previously identified four novel EGFR somatic mutations in the EGFR tyrosine kinase domain of prostate cancer patients: G735S, G796S, E804G and R841K. In this study, we investigated the oncogenic potential of these somatic mutations by establishing stable clonal NIH3T3 cells expressing these four mutations and WT EGFR to determine their ability to increase cell proliferation and invasion. In the absence of the EGF ligand, cell proliferation was readily increased in G735S, G796S and E804G mutants compared to WT EGFR. The addition of EGF ligand greatly increased cell growth and transforming ability of these same EGFR mutants. Matrigel invasion assays showed enhanced invasion with G735S, G796S and E804G mutants. Western blot analysis showed that these EGFR mutations enhanced cell growth and invasion via constitutive and hyperactive tyrosine phosphorylation and led to the activation of mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3 (STAT3) and Akt pathways. Our findings demonstrate the oncogenic activation of three novel EGFR somatic missense mutations in prostate cancer. Molecules that regulate the mechanisms of their oncogenic activation represent novel targets for limiting tumor cell progression, and further elucidation of these mutations will have utility in prostate cancer treatment.

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“…To examine the "paracrine" chemoattractant effects of the VSMC incubation medium on EC invasion of matrix, a standard invasion assay was used (30). The medium from each VSMC experimental condition was added to the bottom of 24-well Falcon TC companion plates.…”

Section: Vascular Endothelial and Smooth Muscle Cellmentioning

confidence: 99%

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

Pedram¹,

Razandi²,

Hu³

et al. 1997

Journal of Biological Chemistry

176

117

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Expression of complete keratin filaments in mouse L cells augments cell migration and invasion.

Cited by 146 publications

References 29 publications

Erythropoietin-mediated activation of JAK-STAT signaling contributes to cellular invasion in head and neck squamous cell carcinoma

Erythropoietin-mediated activation of JAK-STAT signaling contributes to cellular invasion in head and neck squamous cell carcinoma

Epidermal growth factor receptor activation in prostate cancer by three novel missense mutations

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

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