Role of tyrosine specific phosphorylation of cellular proteins, especially EGF receptor and p125FAK in human lung cancer cells

Imaizumi, Munehisa; Nishimura, M; Takeuchi, S; Murase, M; Hamaguchi, Michinari

doi:10.1016/s0169-5002(97)00650-8

Cited by 30 publications

(28 citation statements)

References 17 publications

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“…5 In addition, increased tyrosine phosphorylation of FAK is observed in lung, cervical and ovarian cancers. [17][18][19] Elevated expression of FAK in human tumors has been correlated with increased malignancy and invasiveness. 5,20,21 Mouse transgenic studies show that conditional fak deletion in the epidermis suppresses chemically induced skin tumor formation, and this effect was linked to increased cell apoptosis.…”

Section: Evidence For Fak As a Positive Regulator Of Tumor Cell Migramentioning

confidence: 99%

Paradoxical roles of FAK in tumor cell migration and metastasis

Zheng¹,

Lu²

2009

Cell Cycle

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Section: Evidence For Fak As a Positive Regulator Of Tumor Cell Migramentioning

confidence: 99%

Paradoxical roles of FAK in tumor cell migration and metastasis

Zheng¹,

Lu²

2009

Cell Cycle

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“…These findings were associated with enhanced cell migration (Cary et al, 1996) and proliferation (Wang et al, 2000). In lung cancer, the induced phosphorylation of pp125FAK was positively correlated to lymph node metastasis (Imaizumi et al, 1997). The tumour biological importance of FAK was confirmed by experiments targeting pp125FAK with antisense oligonucleotides leading to an inhibition of cell migration, invasion and proliferation as well as an induction of apoptosis and enhanced sensitivity to campothecins (Hungerford et al, 1996;Golubovskaya et al, 2002;Satoh et al, 2003).…”

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confidence: 94%

Specific induction of pp125 focal adhesion kinase in human breast cancer

et al. 2005

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The pp125 focal adhesion kinase (FAK) is involved in integrin-mediated cell signalling and overexpressed in a variety of solid tumours. Focal adhesion kinase expression has been correlated to invasion and metastasis, but the data on breast cancer are inconclusive. We analysed FAK mRNA, protein levels and expression patterns in primary breast cancer and normal breast tissue. FAK expression on the functional protein level and mRNA was determined in 55 matched pairs of breast cancer and corresponding normal tissue by Western blot, immunohistochemistry and RT -PCR. Using a score ranging from 0 to þ 5 for Western blots, we determined in normal breast tissue a score of 1.5170.84 (mean7standard deviation), which was strongly induced to 2.91 (71.22) in breast cancers (Po0.001). Overall, 45 out of 55 tissue pairs (81.8%) showed this upregulation of FAK protein in tumours in comparison to normal tissue. Immunohistochemistry confirmed these findings with a significant higher score for tumours vs physiological tissue (1.070.63 vs 2.2770.91; P ¼ 0.001). Interestingly, no overall significant difference in the mRNA levels (P ¼ 0.359) was observed. In conclusion, expression levels of the FAK protein are specifically upregulated in breast cancer in comparison to matched normal breast tissue supporting its pivotal role in neoplastic signal transduction and representing a potential marker for malignant transformation.

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“…An association of FAK overexpression and worse clinical prognosis have been reported in a variety of human tumors including those of the colon [5], thyroid [6], ovarian [7], cervix [8], head and neck [9], lung [10], hepatocellular [11], and esophagus [12].…”

Section: Introductionmentioning

confidence: 99%

Clinical significance of high focal adhesion kinase gene copy number and overexpression in invasive breast cancer

Yom

Noh

Kim

et al. 2010

Breast Cancer Res Treat

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Increased expression and activation of focal adhesion kinase (FAK) was reported to be an unfavorable factor in various human cancers, including breast cancer. In order to study FAK gene status as a prognostic factor, we evaluated FAK gene copy number and FAK protein expression in invasive breast cancer. Tumors from 435 patients with invasive breast cancer were evaluated for FAK gene status using fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) based on tissue array method. Survival analyses were performed using the Kaplan-Meier method in 267 patients. 42 out of 362 evaluable cases (11.6%) showed high polysomy and 22 cases (6.1%) had gene amplification by FISH. 108 out of 393 evaluable cases (27.5%) showed FAK overexpression by IHC. FAK FISH positivity was significantly associated with higher histologic grade, higher T stage, negative estrogen receptor expression, negative progesterone receptor expression and triple-negative phenotype; FAK overexpression with higher histologic grade and triple-negative phenotype. FAK overexpression was noted in 57.8% (37 of 64) of FAK FISH+ cases. The concordance of FISH and IHC results for FAK gene was observed in 74.9% (271 of 362). Survival analyses revealed the patients with FAK FISH+ breast cancer had significantly shorter overall survival and relapse-free survival compared to those with FISH- breast cancer. In node-positive breast cancer patients who received postoperative systemic treatment, the patients with FAK FISH+ showed significantly shorter 5-year survival rates. Despite of high significant concordance between the results of FISH and IHC for FAK gene in invasive breast cancer, only FAK FISH positivity was an unfavorable prognostic factor.

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Role of tyrosine specific phosphorylation of cellular proteins, especially EGF receptor and p125FAK in human lung cancer cells

Cited by 30 publications

References 17 publications

Paradoxical roles of FAK in tumor cell migration and metastasis

Paradoxical roles of FAK in tumor cell migration and metastasis

Specific induction of pp125 focal adhesion kinase in human breast cancer

Clinical significance of high focal adhesion kinase gene copy number and overexpression in invasive breast cancer

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