CD9P-1 expression correlates with the metastatic status of lung cancer, and a truncated form of CD9P-1, GS-168AT2, inhibits in vivo tumour growth

Guilmain, William; Colin, Sylvie; Legrand, E; Vannier, Jean‐Pierre; Steverlynck, Céline; Bongaerts, Maud; Vasse, Marc; Al-Mahmood, Salman

doi:10.1038/sj.bjc.6606033

Cited by 21 publications

(20 citation statements)

References 33 publications

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“…In contrast to the reported molecular compensations based on overlapping expressions of tetraspanins, our current work demonstrates an association between tetraspanin and non-tetraspanin molecules to regulate their expressions in an inverse manner. This kind of association has been recently reported in the case of CD9 and CD9P-1, in which the expression of CD9P-1 positively correlates with the metastatic status of lung tumor cells [38]. In the present study, we demonstrated that inverse correlation between CD9 and CD26 play a role on CD9-mediated suppression of invasiveness of CD26-positive tumor cells.…”

Section: Discussionsupporting

confidence: 88%

CD9 Negatively Regulates CD26 Expression and Inhibits CD26-Mediated Enhancement of Invasive Potential of Malignant Mesothelioma Cells

et al. 2014

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CD26/dipeptidyl peptidase IV is a cell surface glycoprotein which consists of multiple functional domains beside its ectopeptidase site. A growing body of evidence indicates that elevated expression of CD26 correlates with disease aggressiveness and invasive potential of selected malignancies. To further explore the molecular mechanisms involved in this clinical behavior, our current work focused on the interaction between CD26 and CD9, which were recently identified as novel markers for cancer stem cells in malignant mesothelioma. We found that CD26 and CD9 co-modulated and co-precipitated with each other in the malignant mesothelioma cell lines ACC-MESO1 and MSTO-211H. SiRNA study revealed that depletion of CD26 led to increased CD9 expression, while depletion of CD9 resulted in increased CD26 expression. Consistent with these findings was the fact that gene transfer of CD26 into CD26-negative MSTO-211H cells reduced CD9 expression. Cell invasion assay showed that overexpression of CD26 or gene depletion of CD9 led to enhanced invasiveness, while CD26 gene depletion resulted in reduced invasive potential. Furthermore, our work suggested that this enhanced invasiveness may be partly mediated by α5β1 integrin, since co-precipitation studies demonstrated an association between CD26 and α5β1 integrin. Finally, gene depletion of CD9 resulted in elevated protein levels and tyrosine phosphorylation of FAK and Cas-L, which are downstream of β1 integrin, while depletion of CD26 led to a reduction in the levels of these molecules. Collectively, our findings suggest that CD26 potentiates tumor cell invasion through its interaction with α5β1 integrin, and CD9 negatively regulates tumor cell invasion by reducing the level of CD26-α5β1 integrin complex through an inverse correlation between CD9 and CD26 expression. Our results also suggest that CD26 and CD9 serve as potential biomarkers as well as promising molecular targets for novel therapeutic approaches in malignant mesothelioma and other malignancies.

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Section: Discussionsupporting

confidence: 88%

CD9 Negatively Regulates CD26 Expression and Inhibits CD26-Mediated Enhancement of Invasive Potential of Malignant Mesothelioma Cells

et al. 2014

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“…Later on, it has been reported to participate in the tetraspanin web [59–61]. Expression of PTGFRN positively correlates with the metastatic status of human lung tumors [62]. However, the function of PTGFR in the metastatic process warrants further studies.…”

Section: Discussionmentioning

confidence: 99%

An optimized isolation of biotinylated cell surface proteins reveals novel players in cancer metastasis

Karhemo

Ravela

Laakso

et al. 2012

Journal of Proteomics

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Details of metastasis, the deadliest aspect of cancer, are unclear. Cell surface proteins play central roles in adhesive contacts between the tumor cell and the stroma during metastasis. We optimized a fast, small-scale isolation of biotinylated cell surface proteins to reveal novel metastasis-associated players froman isogenic pair of human MDA-MB-435 cancer cells with opposite metastatic phenotypes. Isolated proteins were trypsin digested and analyzed using LC–MS/MS followed by quantitation with the Progenesis LC–MS software. Sixteen proteins displayed over twofold expression differences between the metastatic and non-metastatic cells. Interestingly, overexpression of most of them (14/16) in the metastatic cells indicates a gain of novel surface protein profile as compared to the non-metastatic one. All five validated, differentially expressed proteins showed higher expression in the metastatic cells in culture, and four of these were further validated in vivo. Moreover, we analyzed the expression of two of the identified proteins, CD109 and ITGA6 in 3-dimensional cultures of six melanoma cell lines. Both proteins marked the surface of cells derived from melanoma metastasis over cells derived from primary melanoma. These unbiased identification and validation of both known and novel metastasis-associated proteins indicate a reliable approach for the identification of differentially expressed surface proteins.

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“…When the tumor size has reached 80-120 mm 3 , the mice were injected with E2 (0.036 mg/ml, purity 98%, Sigma) or fulvestrant (Ful, 0.800 mg/ml, Sigma) subcutaneously twice a week (6 weeks) [ 11 ]. All mice were then sacrificed on day 45, wherein the xenograft tumors were harvested and the tumor weight and size were measured [ 36 ]. Tumor tissues were fixed in 4% paraformaldehyde or frozen with liquid nitrogen and stored at -80° C.…”

Section: Methodsmentioning

confidence: 99%

Knockdown of CENPF inhibits the progression of lung adenocarcinoma mediated by ERβ2/5 pathway

Tang

Bai

Xiong

et al. 2021

Aging

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Many studies have reported that estrogen (E2) promotes lung cancer by binding to nuclear estrogen receptors (ER), and altering ER related nuclear protein expressions. With the GEO database analysis, Human centromere protein F (CENPF) is highly expressed in lung adenocarcinoma (LUAD), and the co-expression of CENPF and ERβ was found in the nucleus of LUAD cells through immunofluorescence. We identified the nuclear protein CENPF and explored its relationship with the ER pathway. CENPF and ERβ2/5 were related with T stage and poor prognosis (P<0.05). CENPF knockout significantly inhibited LUAD cell growth, the tumor growth of mice and the expression of ERβ2/5 (P<0.05). The protein expression of CENPF and ERβ2/5 in the CENPF-Knockdown+Fulvestrant group was lower than CENPF- Negative Control +Fulvestrant group (P=0.002, 0.004, 0.001) in A549 cells. The tumor size and weight of the CENPF-Knockdown+Fulvestrant group were significantly lower than CENPF- Negative Control +Fulvestrant group (P=0.001, 0.039) in nude mice. All the results indicated that both CENPF and ERβ2/5 play important roles in the progression of LUAD, and knockdown CENPF can inhibit the progression of LUAD by inhibiting the expression of ER2/5. Thus, the development of inhibitors against ERβ2/5 and CENPF remained more effective in improving the therapeutic effect of LUAD.

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CD9P-1 expression correlates with the metastatic status of lung cancer, and a truncated form of CD9P-1, GS-168AT2, inhibits in vivo tumour growth

Cited by 21 publications

References 33 publications

CD9 Negatively Regulates CD26 Expression and Inhibits CD26-Mediated Enhancement of Invasive Potential of Malignant Mesothelioma Cells

CD9 Negatively Regulates CD26 Expression and Inhibits CD26-Mediated Enhancement of Invasive Potential of Malignant Mesothelioma Cells

An optimized isolation of biotinylated cell surface proteins reveals novel players in cancer metastasis

Knockdown of CENPF inhibits the progression of lung adenocarcinoma mediated by ERβ2/5 pathway

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