Epidermal growth factor inhibits growth of A431 human epidermoid carcinoma in serum-free cell culture.

Barnes, David W.

doi:10.1083/jcb.93.1.1

Cited by 260 publications

(144 citation statements)

References 31 publications

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“…Thus, the situation of ATL leukemia cells seems to be similar to that of the TL cell lines in which growth was inhibited by IL-2. The growth of epidermoid carcinoma cell lines such as A431 is also suppressed by EGF (15,16), although EGF promoted the growth of various EGF receptor-bearing primary epidermal ceils (17). These observations seem very similar to the present observations on the interaction between IL-2 and TL cells.…”

Section: Discussionsupporting

confidence: 89%

Interleukin 2 inhibits in vitro growth of human T cell lines carrying retrovirus.

Sugamura¹,

Nakai²,

Fujii³

et al. 1985

The Journal of Experimental Medicine

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Human T cell leukemia virus (HTLV), which we previously called adult T cell leukemia virus (ATLV), is a possible causative agent of human adult T cell leukemia (ATL) (1). Since the HTLV genome was demonstrated not to contain a typical v-onc gene (2) and the HTLV proviral genome is integrated into random sites in cellular DNA of leukemia cells in each ATL patient (3), the mechanism of HTLV-induced oncogenesis is still unknown. The interleukin 2 (IL-2) autocrine hypothesis can be excluded as the mechanism of ATL leukemogenesis, because the IL-2 receptor (IL-2R) was detected in all ATL leukemia cells and HTLV-transformed human T cells that were examined (4), but the IL-2 gene was not transcribed in most of these cells (5). However, it was reported (6) that expression of the IL-2R is abnormal in ATL leukemia cells because it is not down-regulated by anti-IL-2R (Tac) antibody, and is constitutive, while IL-2R expression in peripheral blood leukocytes (PBL) stimulated with concanavalin A is down-regulated. This observation resulted in another hypothesis, that the constitutive expression of the IL-2R may play a crucial role in ATL leukemogenesis. Our recent observation (7) that HTLV can induce expression of the IL-2R on human B cell lines, strongly supports the notion that HTLV directly contributes to the constitutive production of the IL-2R on ATL leukemia cells and other HTLV-carrying human T cells. However, it is still unknown how the cell growth signal can be transduced constitutively from the IL-2R expressed on ATL leukemia cells and HTLV-transformed cell lines. Similarly, it has been demonstrated (8) that the A431 human epidermoid carcinoma cell line has a large number of receptors for the epidermal growth factor (EGF) that could be products of the c-erbB gene, a cellular oncogene, and it is suggested (8) that overproduction or uncontrolled expression of the EGF receptors could be related to the appearance of the transformed phenotype in the A431 cell line.We previously (4) obtained HTLV-carrying human T cell lines of two distinct types with respect to their IL-2 dependency. One type (ILT) is IL-2 dependent; the other (TL) is IL-2 independent for in vitro growth. Most of the IL-2-independent TL cell lines arose spontaneously from IL-2-dependent ILT cell lines in vitro. This change from IL-2 dependence to IL-2 independence could be due to immortalizing transformation of the cells induced by HTLV (9, 10).

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Section: Discussionsupporting

confidence: 89%

Interleukin 2 inhibits in vitro growth of human T cell lines carrying retrovirus.

Sugamura¹,

Nakai²,

Fujii³

et al. 1985

The Journal of Experimental Medicine

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“…This is consistent with data from squamous cell lines of other histologies, such as A431 cells, where EGF, when added at nanomolar concentrations, is inhibitory to systems showing very high concentrations of the EGF receptor although, if added at picomolar concentrations, EGF can be stimulatory (Gill & Lazar, 1981;Barnes, 1982;Filmus et a!., 1985;Kamata et al, 1986). In several studies the level of inhibition has been shown to increase as the EGF receptor number increases (Kamata et al, 1986;.…”

Section: Discussionsupporting

confidence: 87%

Growth control by epidermal growth factor and transforming growth factor-α in human lung squamous carcinoma cells

Rabiasz

Langdon²,

Bartlett³

et al. 1992

Br J Cancer

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Summary Although EGF receptor expression is generally elevated in human lung squamous carcinoma, the biological significance of this phenomenon and the role of EGF and TGF-a in this disease are poorly understood. We have investigated three human lung squamous carcinoma cell lines (NX002, CX140 and CX143) and have shown, using an antibody (EGFRI) directed against the EGF receptor, that the majority of cells in all three lines express the EGF receptor. Using a ligand binding assay, Scatchard analysis indicated high concentrations (1,300-2,700 fmol mg-' protein) of a single low affinity binding site (Kd = 3-5 nM) within these lines. Addition of EGF or TGF-a at concentrations greater than 0.1 nm resulted in growth inhibition of all three lines and this was associated with an accumulation of cells in the G2/M phase of the cell cycle. Growth inhibitory effects were not explained by an enhancement of cellular differentiation as monitored by involucrin expression and the ability to form cornified envelopes. While the presence of EGF could not be detected in medium conditioned by the NX002 cell line, mRNA for TGF-a was detected in all three lines suggesting the possibility of an autocrine loop. These results together with reports of growth inhibition by EGF and TGF-a in other systems suggest that EGF and similar molecules might have a growth regulatory role in lung cancer cells and modulation of such may have therapeutic potential.The related molecules, epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-ax), modulate the growth of a wide variety of normal and malignant cells (reviewed in Burgess et al., 1989). Both factors operate through the EGF receptor and in many malignant diseases, for example lung squamous carcinoma, levels of the EGF receptor are markedly overexpressed relative to normal tissue (Hendler & Ozanne, 1984;Cerny et al., 1986;Berger et al., 1987;Veale et al., 1987;Sobol et al., 1987;Dazzi et al., 1989). The biological significance of this overexpression of receptors in lung squamous carcinoma is not known. Cell lines derived from human lung squamous carcinoma cell lines have been shown to possess high concentrations of EGF receptors (Haeder et al., 1988) and represent useful models to study growth factor modulation. Little is known of the role of EGF and TGF-x in this disease, however, several reports have proposed that TGF-o may act in an autocrine manner in this cell type (Lee et al., 1990;Putnam et al., 1991) while another recent study has suggested that either EGF or TGFa might stimulate squamous differentiation (Levitt et al., 1991).In order to investigate further the role of EGF-like factors in lung squamous carcinoma cells, we have developed cell line models and have examined them for the presence of EGF receptors. Two approaches have been used to detect and measure the levels of this receptor: immunocytochemical staining using an antibody directed against the receptor and a competitive binding assay employing radiolabelled EGF. We have also studied the effects of EGF and T...

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“…These data are at variance with those of others which suggest that either EGF-R expression is decreased in hepatoma cells [27], or that abnormal expression of the EGF-R of HCC-cells is not among the factors responsible for the aberrant cell proliferation [15]. EGF has been observed to inhibit growth in vitro of a variety of carcinoma-derived cell lines [28][29][30][31], most of which exhibit high levels of high-affinity EGF receptors as a consequence of gene amplification. It has been proposed that this EGF-linked inhibition of cell replication may be due to excessive kinase stimulation, which depletes cellular energy stores [32].…”

Section: Discusionmentioning

confidence: 54%

Expression of high‐ and low‐affinity epidermal growth factor receptors in human hepatoma cell lines

Clementi¹,

Festa

Testa

et al. 1989

FEBS Letters

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Data are presented from a comparative research on expression of epidermal growth factor (EGF) receptors and response to EGF of six independently established cell lines derived from human hepatoma. These lines differ in terms of the degree of differentiation, presence of hepatitis B virus (HBV) DNA copies in integrated form and expression of HBV genes. Our results indicate differential expression of membrane EGF receptors and differential response to EGF under serumand hormone-free culture conditions. Furthermore, a significant difference in affinity could be detected between EGF receptors of the two highly dedifferentiated cell lines (HA22T/VGH and Li7A) whose replication is inhibited by EGF concentrations capable of stimulating more differentiated phenotypes.Epidermal growth factor receptor; Cell replication; (Human hepatoma cell)

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Epidermal growth factor inhibits growth of A431 human epidermoid carcinoma in serum-free cell culture.

Cited by 260 publications

References 31 publications

Interleukin 2 inhibits in vitro growth of human T cell lines carrying retrovirus.

Interleukin 2 inhibits in vitro growth of human T cell lines carrying retrovirus.

Growth control by epidermal growth factor and transforming growth factor-α in human lung squamous carcinoma cells

Expression of high‐ and low‐affinity epidermal growth factor receptors in human hepatoma cell lines

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