Osteopontin is linked to p65 and MMP‐9 expression in pulmonary adenocarcinoma but not in malignant pleural mesothelioma

Frey, Amy; Wali, Anil; Pass, Harvey I.; Lonardo, Fulvio

doi:10.1111/j.1365-2559.2007.02675.x

Cited by 18 publications

(15 citation statements)

References 40 publications

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“…Furthermore we did not find a difference in serum OPN levels between squamous cell and adenocarcinoma. This is in contrast to the findings of another study showing that OPN levels of squamous cell carcinoma were significantly higher than those of adenocarcinoma (25).…”

Section: Serumcontrasting

confidence: 99%

Serum osteopontin in patients with lung cancer and chronic obstructive pulmonary disease: does the co-existence make the difference?

et al. 2018

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Section: Serumcontrasting

confidence: 99%

Serum osteopontin in patients with lung cancer and chronic obstructive pulmonary disease: does the co-existence make the difference?

et al. 2018

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“…Interestingly, elevated OPN expression correlate with MMP-9 levels (33) and MMP-9 mediates OPN-induced cell migration and chemoinvasion in B16F10 cells (34). In PC3 cells, OPN overexpression increases MMP-9 activity (17), presenting strong evidence that MMP-9 is a downstream effector of OPN in invasion.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Biphasic Role for Genistein in the Regulation of Prostate Cancer Growth and Metastasis

Touny

Banerjee

2009

Cancer Research

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Considered a chemopreventive agent, the ability of genistein to modulate the progression of existing prostate cancer (CaP) is not clear. We show here that the consumption of genistein (250 mg/kg diet) by 12-week-old transgenic adenocarcinoma mouse prostate (TRAMP-FVB) mice harboring prostatic intraepithelial neoplasia lesions until 20 weeks of age induces an aggressive progression of CaP, as evidenced by a 16% increase in the number of well-differentiated and poorly differentiated prostates, coinciding with a 70% incidence of pelvic lymph node (LN) metastases as opposed to 0% and 10% in 0 and 1,000 mg/kg groups, concomitant with elevated osteopontin (OPN) expression in prostates and LNs. Equivalent nanomolar (500 nmol/L) concentrations of genistein recapitulated these effects in human PC3 CaP cells as evidenced by increased proliferation, invasion, and matrix metalloproteinase-9 (MMP-9) activity (f2-fold), accompanied by an up-regulation of OPN expression and secretion, compared with vehicletreated cells. A pharmacologic dose (50 Mmol/L) decreased proliferation, invasion, and MMP-9 activity (>2.0-fold) concomitant with OPN reduction. Upon OPN knockdown by short hairpin RNA, genistein was no longer effective in upregulating PC3 cell proliferation, invasion, and MMP-9 activation, which were significantly reduced in the absence of OPN, highlighting the requirement for OPN in mediating the effects of genistein. Proliferation, invasion, and OPN levels were also nonsignificantly induced by genistein in the presence of ICI 182,780 or wortmannin, indicating a dependence on phosphatidylinositol 3-kinase and estrogen signaling. Our results suggest the presence of a biphasic regulation of CaP growth and metastasis by genistein, warranting careful examination of the effects of genistein on hormone-dependent cancers in a chemotherapeutic setting. [Cancer Res 2009;69(8):3695-703]

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“…Osteopontin (OPN) is a multifunctional protein that has been implicated in the pathogenesis of numerous conditions, including malignant transformation, autoimmune diseases, and pulmonary fibrosis (12)(13)(14)(15). OPN elevations have also been described in smokers, where levels correlated with degree of airway obstruction (16).…”

mentioning

confidence: 98%

Adenosine and osteopontin contribute to the development of chronic obstructive pulmonary disease

et al. 2009

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Chronic obstructive pulmonary disease (COPD) is a major health concern. Adenosine, a signaling molecule generated in response to cell stress, contributes to the pathogenesis of COPD. An established model of adenosine-mediated lung injury is the adenosine deaminase-deficient (Ada(-/-)) mouse. Osteopontin (OPN) is a chemokine that is produced following injury and is implicated in a variety of human pathologies, but its expression and role in the pathogenesis of COPD have not been examined. To investigate the role of OPN in a model of COPD, Ada(-/-) double-knockout mice were generated, and inflammation and air-space enlargement endpoints were examined. Results demonstrate that Ada(-/-) mice exhibit OPN-dependent neutrophilia, alveolar air-space enlargement, and increases in mediators of air-space enlargement. Furthermore, we demonstrate that patients with COPD have increased OPN expression within distal airways in association with clinical airway obstruction. These results suggest that OPN represents a novel biomarker and therapeutic target for patients with COPD.

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Osteopontin is linked to p65 and MMP‐9 expression in pulmonary adenocarcinoma but not in malignant pleural mesothelioma

Abstract: Frequent OPN expression is typical of, but not specific for MM, whereas it appears to select adenocarcinoma cases with p65 and MMP-9 expression, suggesting a link with EGFR signalling pathways.

Cited by 18 publications

References 40 publications

Serum osteopontin in patients with lung cancer and chronic obstructive pulmonary disease: does the co-existence make the difference?

Serum osteopontin in patients with lung cancer and chronic obstructive pulmonary disease: does the co-existence make the difference?

Identification of a Biphasic Role for Genistein in the Regulation of Prostate Cancer Growth and Metastasis

Adenosine and osteopontin contribute to the development of chronic obstructive pulmonary disease

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