Preferential histiotypic expression of CD44-isoforms in human lung cancer

Wimmel, Anja; Schilli, M.; Kaiser, Ulrich; Havemann, K.; Ramaswamy, A.; Branscheid, D.; Kogan, E. A.; Schuermann, Marcus

doi:10.1016/s0169-5002(96)00625-3

Cited by 20 publications

(19 citation statements)

References 24 publications

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“…John et al, 1990;Weber et al, 1996). Our ®nding that CD44 is preferentially expressed in NSCLC cell lines also is in line with previous reports which show that CD44 is preferentially expressed in NSCLC-type tumors but not in SCLC (Givehchian et al, 1996;Penno et al, 1994;Wimmel et al, 1997) and as such can be viewed as an NSCLC-speci®c marker. In the light of these data also the NSCLC character of H-ras/ c-myc transfected SCLC clones is supported.…”

Section: Discussionsupporting

confidence: 90%

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Transition from SCLC to NSCLC phenotype is accompanied by an increased TRE-binding activity and recruitment of specific AP-1 proteins

et al. 1998

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Transitions from small cell (SCLC) to non-small cell lung cancer (NSCLC) cells have been documented both in vitro and in vivo and are thought to be an important step during tumor progression of human small cell lung cancer towards a treatment-resistant tumor state. We have screened NSCLC and SCLC cell lines for dierences in the composition of nuclear transcription factors using consensus oligonucleotide sequences (SRE, Ets, TRE, CRE, B-motif, GAS, E-box). We found NSCLC cells to exhibit signi®cantly higher AP-1 binding activity than SCLC cells consistent with the increased expression of CD44, an AP-1 target gene. To gain more insight into the molecular mechanisms underlying these dierences, we analysed SCLC cell lines (NCI-N592 and NCI-H69) which were phenotypically transformed into NSCLC-type cells by transfection with activated H-ras and c-myc oncogenes. In these cells, ras-induced transition is accompanied by a strong induction of AP-1-binding activity along with increased expression of CD44 mRNA and protein. When analysing the composition of the AP-1 complex in more detail and comparing ras-induced versus phorbol ester-induced changes, we found Fra-1 to be the major component induced in ras-transfected but not in phorbol-ester treated or non-treated parental SCLC cells. This ®nding is paralleled by the observation that among the various members of the Fos and Jun family analysed (c-Fos, FosB, Fra-1, Fra-2, c-Jun, JunD, JunB) fra-1 is the only gene to be exclusively expressed in NSCLC cells but not in cells of SCLC origin. Our data, thus, point to a histiotype-related mechanism of recruitment among AP-1 proteins which may have bearings on the fate of lung cancer development.

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Section: Discussionsupporting

confidence: 90%

“…The origin and characteristics of these cell lines have been described previously (Wimmel et al, 1997). All cells were grown in RPMI 1640 medium (GIBCO ± BRL) supplemented with 10% heat-inactivated fetal calf serum (GIBCO ± BRL), nonessential amino acids and 4 mmol/L glutamine.…”

Section: Cell Linesmentioning

confidence: 99%

Transition from SCLC to NSCLC phenotype is accompanied by an increased TRE-binding activity and recruitment of specific AP-1 proteins

et al. 1998

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“…What pointed toward layilin as an ideal HA receptor to be involved epithelial permeability is that it is known to interact with members of the ezrin, radixin, and moesin proteins (81) that are key regulators of cytoskeletonplasma membrane interactions in polarized cell. CD44 and RHAMM are two of the better characterized HA receptors in airway epithelial cells (19,21,(82)(83)(84), but in intact epithelium CD44 expression is restricted to the basolateral domain (83,85,86) and thus, at least initially, cannot be accessed by fragments released during luminal HA degradation. RHAMM is apically expressed (19,21) but lacks a cytoplasmic domain.…”

Section: Discussionmentioning

confidence: 99%

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

Forteza

Casalino‐Matsuda

Falcon

et al. 2012

Journal of Biological Chemistry

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Background: Cigarette smoke (CigS) induces hyaluronan fragmentation and increases epithelial permeability. Results: CigS and HA fragments decrease E-cadherin expression that is prevented by knocking down layilin. Conclusion: HA fragments bind to layilin and signal through RhoA/ROCK to inhibit E-cadherin. Significance: Airway epithelium is our first line of defense against inhaled insults. HA fragments released by CigS disrupt this barrier.

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“…Differential gene expression analysis showed that expression of a variety of characteristic c-SCLC neuroendocrine markers , including chromogranin A, L-dopa-decarboxylase, NSE and bombesin were lost or diminished in the adherent sublines, while NSCLC markers such as CD44 (Wimmel et al, 1997) and cyclin D1 (Schauer et al, 1994) were up-regulated. Since this mirrors the pattern of expression seen in vivo in variant SCLC cells, spontaneously adherent SCLC sublines can be said to Figure 4 (a) and (b) Dose-dependent sensitivities of NCI-N592 and the adherent subline N592ad to each of etoposide, cyclophosphamide, doxorubicin and paclitaxel treatments.…”

Section: Discussionmentioning

confidence: 99%

In vitro chemo- and radio-resistance in small cell lung cancer correlates with cell adhesion and constitutive activation of AKT and MAP kinase pathways

et al. 2002

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Most small cell lung cancer (SCLC) patients relapse within 12 months of starting combination chemotherapy plus radio-therapy, due to the development of acquired chemo-and radio-resistance. This phenomenon relates to the induction of tumour differentiation, resulting in apoptosis-resistant, morphologically variant (v-SCLC) cells, which lack the neuroendocrine expression of classic (c-) SCLC cells. In this study spontaneously adherent SCLC sublines were shown by differential gene expression analysis to provide an in vitro model of variant differentiation in SCLC, with down-regulation of neuroendocrine markers and up-regulation of epithelial differentiation markers cyclin D1, endothelin, the cell adhesion molecules CD 44 and integrin subunits a2, b3 and b4. The sensitivity of adherent SCLC sublines to etoposide, cyclophosphamide and gamma radiation was significantly diminished relative to parent suspension cell lines. Western blot analysis using phosphorylationspecific antibodies to Akt and MAP kinase revealed markedly elevated activation in adherent SCLC sublines, paralleled by increased levels of phosphorylated Bad protein and activated NF-kB. Subcultivation of the adherent sublines on uncoated surfaces reversed their adherent phenotype immediately and under these conditions Akt activity reverted to low levels. These results suggest that c-SCLC cells can differentiate spontaneously to v-SCLC and that the associated cellular adhesion may trigger Akt-dependent inhibition of apoptosis in SCLC cells, thus leading to acquired chemoand radio-resistance.

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Preferential histiotypic expression of CD44-isoforms in human lung cancer

Cited by 20 publications

References 24 publications

Transition from SCLC to NSCLC phenotype is accompanied by an increased TRE-binding activity and recruitment of specific AP-1 proteins

Transition from SCLC to NSCLC phenotype is accompanied by an increased TRE-binding activity and recruitment of specific AP-1 proteins

Hyaluronan and Layilin Mediate Loss of Airway Epithelial Barrier Function Induced by Cigarette Smoke by Decreasing E-cadherin

In vitro chemo- and radio-resistance in small cell lung cancer correlates with cell adhesion and constitutive activation of AKT and MAP kinase pathways

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