EGF Induces Cell Motility and Multi-Drug Resistance Gene Expression in Breast Cancer Cells

García, R.; Franklin, Richard A.; McCubrey, James A.

doi:10.4161/cc.5.23.3535

Cited by 65 publications

(55 citation statements)

References 35 publications

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“…EGF over-expression could increase cell differentiation and proliferation, inhibit apoptosis and enhance invasiveness of cancer cells in many tumor types, including breast cancer [10][11][12][13]. The EGF gene contains an atypical TATA box, polypurine-rich motifs and consensus binding sequences for many transcription factors, e.g., NF-kB, GAS, AP-1, Sp1, C/EBP, etc.…”

Section: Introductionmentioning

confidence: 99%

EGF promoter SNPs, plasma EGF levels and risk of breast cancer in Chinese women

Wang

Tian

et al. 2007

Breast Cancer Res Treat

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Epidermal growth factor (EGF), a potent mitogenic peptide, plays an important role in the development of cancers, including breast cancer. Previous studies showed that plasma EGF levels may influence the risk of cancer. In the current study, we hypothesized that genetic variants in the promoter region of EGF may influence plasma EGF levels and therefore are associated with breast cancer susceptibility. We genotyped three EGF polymorphisms (G61A, G-1380A, and A-1744G) in the promoter region by PCR-RFLP and measured plasma EGF levels using an enzyme immunoassay in a case-control study of Chinese women. We found that the mean plasma EGF levels in breast cancer patients (249.06 +/- 197.54 pg/ml) were significantly lower than those in controls (982.41 +/- 375.57 pg/ml, P < 0.001). There was a significant difference of plasma EGF levels among different genotypes carriers of the G-1380A locus in 654 controls (P = 0.007). After adjustment for age, body mass index, family history of cancer, age at menarche, and menopause status, EGF-1380AA carriers had significantly higher plasma EGF levels than -1380GG carriers did (P = 0.003). However, we did not find any significant associations between the three EGF polymorphisms (G61A, G-1380A, and A-1744G) and the risk of breast cancer. These findings indicated that plasma EGF levels served as a protective marker against breast cancer in our study and EGF G-1380A variant might be a modifier on it. Further studies are warranted to verify these findings.

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Section: Introductionmentioning

confidence: 99%

EGF promoter SNPs, plasma EGF levels and risk of breast cancer in Chinese women

Wang

Tian

et al. 2007

Breast Cancer Res Treat

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“…[276][277][278] Recently, we and others have shown that aberrant activity of the PI3K/PTEN/Akt/mTOR signaling cascade can augment drug resistance in advanced CaP cells. 279,280 These reports detail several potential mechanisms responsible for increased chemoresistance including PI3K-induced overexpression of the MRP-1 drug pump as well as activation of the mTOR molecule that is downstream of PI3K/Akt.…”

Section: Treatment Of Prostate Cancermentioning

confidence: 99%

Targeting prostate cancer based on signal transduction and cell cycle pathways

Lee¹,

Lehmann²,

Terrian³

et al. 2008

Cell Cycle

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“…40 Our data showed that VCR increased the expressions of P-gp and MRP1 in HepG2 cells, and these upregulations were impaired by pCSH1-shNR. It was because that the expression levels of P-gp and MRP1 were regulated by ERKs and Akt, which were inhibited by pCSH1-shNR, 40,41 and the promoter of human MDR1 gene was shown to be a target for Ras. 42,43 Moreover, Ras-mediated activation of the MEK/MAP kinase pathway increases cellular levels of cyclin D1, but other effector pathways may also be important in cyclin D1 induction.…”

Section: Discussionmentioning

confidence: 99%

Suppression of N-Ras by shRNA-expressing plasmid increases sensitivity of HepG2 cells to vincristine-induced growth inhibition

et al. 2009

Cancer Gene Ther

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Oncogenic ras genes relate to the development of human cancers. In this study, we used a plasmid-mediated short-hairpin RNA (shRNA) targeting N-ras gene to combine with clinical drug vincristine (VCR) for the treatment of human hepatoma cells. Our results showed that anti-N-Ras shRNA expression vector (pCSH1-shNR) knocked down the target mRNA and protein. Higher efficacy on growth inhibition was observed when pCSH1-shNR was combined with VCR. This synergistic effect was associated with abrogation of VCR-induced overexpressions of P-glycoprotein and multidrug resistance-associated protein 1 by pCSH1-shNR through downregulations of N-Ras and total Ras. Western blot analysis showed that pCSH1-shNR-induced downregulations of N-Ras and total Ras were potentiated by VCR. Following Ras downregulation, phosphorylations of ERK1/2 and Akt were dramatically inhibited by combinatory treatment. The data showed that pCSH1-shNR-induced inhibition of nuclear factor-kB was enhanced by VCR. In addition, the combination of pCSH1-shNR and VCR synergistically inhibited the growth of human hepatoma HepG2 in vivo. Our findings suggested that combination of gene-specific therapeutics and appropriate chemotherapeutic agents might be a promising approach for the treatment of human hepatocellular carcinoma.

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EGF Induces Cell Motility and Multi-Drug Resistance Gene Expression in Breast Cancer Cells

Cited by 65 publications

References 35 publications

EGF promoter SNPs, plasma EGF levels and risk of breast cancer in Chinese women

EGF promoter SNPs, plasma EGF levels and risk of breast cancer in Chinese women

Targeting prostate cancer based on signal transduction and cell cycle pathways

Suppression of N-Ras by shRNA-expressing plasmid increases sensitivity of HepG2 cells to vincristine-induced growth inhibition

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