Expression of transforming growth factor alpha messenger rna in the normal and neoplastic gastro‐intestinal tract

Malden, L.T.; Novak, Ulrike; Burgess, Anthony W

doi:10.1002/ijc.2910430305

Cited by 130 publications

(73 citation statements)

References 33 publications

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“…Elevated levels of EGFR have been demonstrated in many different types of cancer including glioblastoma, and EGFR overexpression seems to be associated with poor prognosis in several neoplasms (3). EGFR overexpression is often associated with gene amplification (4)(5)(6)(7)(8). In glioblastoma, EGFR amplification has been shown to be accompanied by gene rearrangement (9)(10)(11), frequently with deletions in the coding region.…”

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confidence: 99%

A monoclonal antibody recognizing human cancers with amplification/overexpression of the human epidermal growth factor receptor

Jungbluth

Stockert

Huang

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

160

130

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CorrectionsArai, and Glenn D. Prestwich, which appeared in number 1, January 7, 2003, of Proc. Natl. Acad. Sci. USA (100, 131-136; First Published December 26, 2002; 10.1073͞pnas.0135855100), Fig. 4 should have appeared in color. The correct figure and its legend appear below. Fig. 4.LPA stimulates lipid accumulation, CD36 expression, and oxidized LDL uptake through a PPAR-responsive element. (a) LPA stimulates monocyte uptake of oxidized LDL. Freshly elutriated human monocytes were allowed to interact with an anti-ICAM3-coated well, which leads to rapid PPAR␥ expression (13), and then stimulated, or not (negative, oxLDL), with oleoyl LPA. Some cells were then briefly exposed to oxidized LDL before intracellular lipid stores were visualized with oil red O stain. (b) LPA increases the expression of CD36 on the surface of primary human monocytes. Monocytes engaging anti-ICAM3 were treated or not with LPA, and then recovered by gentle scraping and washing by centrifugation before their surface CD36 was assessed by flow cytometry. (c) LPA and the LPA analogs XY4 and XY8 stimulate CD36 promoter function only when the PPRE is present. RAW264.7 cells were transfected with the human CD36 promoter containing the PPRE (CD36 Ϫ273 ) or a reporter that lacks only this element (CD36 Ϫ261 ) and then stimulated with oleoyl LPA, azPC, XY4, or XY8. Expression of luciferase normalized to ␤-galactosidase was determined as above. (d) Anti-CD36 blocks LPA-stimulated accumulation of cholesterol from oxidized LDL. Freshly isolated human monocytes were treated as in a, but after being preincubated with a blocking anti-CD36 antibody before exposure to oxidized LDL. G rowth factor receptors are promising targets for antibodybased cancer therapies. Because of their cell-surface location, they are readily accessible, and therapeutic antibodies can exert their inhibitory effects by either interfering with cellular signaling or targeting toxic molecules or biological effectors to the tumor site (1).The epidermal growth factor receptor (EGFR) is expressed in normal tissues and neoplastic lesions of most organs, and its expression level has been associated with biological characteristics of tumors (2). Elevated levels of EGFR have been demonstrated in many different types of cancer including glioblastoma, and EGFR overexpression seems to be associated with poor prognosis in several neoplasms (3). EGFR overexpression is often associated with gene amplification (4-8). In glioblastoma, EGFR amplification has been shown to be accompanied by gene rearrangement (9-11), frequently with deletions in the coding region. Several mutant forms have been found (12, 13), and among these the most common mutation is the ⌬2-7 deletion (⌬EGFR), which lacks exons 2-7 of the external EGFR domain, resulting in the loss of an 801-bp fragment of the wild-type (wt) gene (14). Several studies have indicated that the presence of ⌬EGFR enhances the tumorigenic behavior of cancer cells (15-17). ⌬EGFR has only been found in neoplastic lesions and not in any normal tissue. ...

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confidence: 99%

A monoclonal antibody recognizing human cancers with amplification/overexpression of the human epidermal growth factor receptor

Jungbluth

Stockert

Huang

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

160

130

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“…A number of epithelial tumor cells with increased expression of EGFR also produce its ligands, and therefore, leading to enhanced autocrine growth stimulation Van de Vijver et al, 1991;Atlas et al, 1992). EGFR and TGF-alpha are expressed in human colorectal carcinomas (Malden et al, 1989) and in a number of colorectal carcinoma-derived human cell lines (Co ey et al, 1986;Markowitz et al, 1990;Untawalwe et al, 1993). In recent years, approaches involving interference with and/or blocking of EGFRmediated autocrine growth stimulation by anti-EGFR mAbs have been the subject of active investigation in an e ort to control cell proliferation (Mendelsohn 1990).…”

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confidence: 99%

Nuclear targeting of Bax during apoptosis in human colorectal cancer cells

et al. 1998

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Homeostasis in colonic epithelial cells is regulated by the balance between proliferative activity and cell loss by apoptosis. Because epithelial cells at the apex of colonic crypts undergo apoptosis and proliferative activity is usually restricted to the base of the crypts, it has been proposed that the limited availability of growth factorsignals at the upper portions of the crypts may trigger apoptosis. In the present studies, we investigate the mechanism of apoptosis mediated by growth factor deprivation in colorectal carcinoma cells by delineating the possible involvement of Bax and its subcellular localization. We report that inhibition of epidermal growth factor receptor (EGFR) tyrosine kinase activity and downregulation of EGFR by anti-EGFR mAb 225 induces apoptosis in human colorectal carcinoma DiFi and FET cells. Induction of apoptosis was preceded by enhanced expression of newly synthesized Bax protein, and required protein synthesis. In the mAb 225-treated cells, Bax was redistributed from the cytosol to the nucleus and subsequently, to the nuclear membranes. The observed induction of Bax expression by mAb 225 was not associated with p53 induction. However, mAb 225 treatment also triggered relocalization of p53 from the cytosol to a nuclear membrane-bound form. Induction of Bax and its redistribution to the nucleus of DiFi cells during apoptosis was also demonstrated in response to butyrate, a physiological relevant molecule in colonic epithelial cells as it is the principal short-chain fatty acid produced by bacterial fermentation of dietary ®ber in colonic epithelium. Using immuno¯uorescence and confocal microscopy, we observed that Bax is predominantly localized in the cytosol, but during apoptosis it is localized both inside and along the nuclear membrane. Taken together, these ®ndings suggest that apoptosis induced by growth factor-deprivation or butyrate may involve the subcellular redistribution of Bax in human colorectal carcinoma cells.

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“…For instance, transfection to achieve co-expression of TGF-a and EGFR results in transformation of fibroblast cell lines (Di Marco et al, 1989). Although TGF-a expression has also been detected in normal colon (Malden et al, 1989), co-expression of TGF-a and EGFR and growth stimulation by TGF-a has been demonstrated in multiple colon cancer cell lines (Mulder and Brattain, 1989). Overexpression of EGFR has been reported in squamous cell carcinoma of the skin, oesophagus (Itakura et al, 1994;Stanton et al, 1994), non-small-cell lung carcinoma (Rusch et al, 1993), breast adenocarcinoma and endometrial adenocarcinoma (Khalifa et al, 1994;Miller et al, 1994).…”

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Epidermal growth factor receptor expression in primary cultured human colorectal carcinoma cells

Ellinger²,

Sheinin³

et al. 1998

Br J Cancer

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Summary In situ hybridization on human colon tissue demonstrates that epidermal growth factor receptor (EGFR) mRNA expression is strongly increased during tumour progression. To obtain test systems to evaluate the relevance of growth factor action during carcinogenesis, primary cultures from human colorectal carcinomas were established. EGFR distribution was determined in 2 of the 27 primary cultures and was compared with that in well-defined subclones derived from the Caco-2 cell line, which has the unique property to differentiate spontaneously in vitro in a manner similar to normal enterocytes. The primary carcinoma-derived cells had up to three-fold higher total EGFR levels than the Caco-2 subclones and a basal mitotic rate at least fourfold higher. The EGFR affinity constant is 0.26 nmol 1-1, which is similar to that reported in Caco-2 cells. The proliferation rate of Caco-2 cells is mainly induced by EGF from the basolateral cell surface where the majority of receptors are located, whereas primary cultures are strongly stimulated from the apical side also. This corresponds to a three-to fivefold higher level of EGFR at the apical cell surface. This redistribution of EGFR to apical plasma membranes in advanced colon carcinoma cells suggests that autocrine growth factors in the colon lumen may play a significant role during tumour progression.

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Expression of transforming growth factor alpha messenger rna in the normal and neoplastic gastro‐intestinal tract

Cited by 130 publications

References 33 publications

A monoclonal antibody recognizing human cancers with amplification/overexpression of the human epidermal growth factor receptor

A monoclonal antibody recognizing human cancers with amplification/overexpression of the human epidermal growth factor receptor

Nuclear targeting of Bax during apoptosis in human colorectal cancer cells

Epidermal growth factor receptor expression in primary cultured human colorectal carcinoma cells

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