Reversion-inducing cysteine-rich protein with Kazal motif (RECK) expression: an independent prognostic marker of survival in colorectal cancer

Winterfeld, Moritz von; Rabien, Anja; Warth, Arne; Kamphues, Carsten; Dietel, Manfred; Weichert, Wilko; Klauschen, Frederick; Wittschieber, Daniel

doi:10.1016/j.humpath.2011.10.012

Cited by 18 publications

(16 citation statements)

References 33 publications

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“…RECK, however, contains diagnostic potential as we could demonstrate a strong decrease in RCC as compared to adjacent normal tissue. This decrease was more pronounced than in prostate carcinoma [14,19] and fits also well to findings for colorectal cancer [15] and other tumor entities (reviewed in [20,21]).…”

Section: Discussionsupporting

confidence: 86%

“…RECK and EMMPRIN were mostly localized as expected. RECK was found with cytoplasmic granular staining as shown for prostate carcinoma [14], urothelial bladder carcinoma [6] and colorectal carcinoma [15], although membranous staining described for the other tumor entities was not prominent. EMMPRIN, however, was mainly localized at the plasma membrane, consistent with our findings for urothelial bladder carcinoma [6] and colorectal carcinoma [16] and consistent with other studies, among them studies on human kidney tissue [9,17] and RCC [7,8,10,18].…”

Section: Discussionmentioning

confidence: 99%

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Renal cell neoplasias: reversion-inducing cysteine-rich protein with Kazal motifs discriminates tumor subtypes, while extracellular matrix metalloproteinase inducer indicates prognosis

Rabien

Stephan

Kilic

et al. 2013

Journal of Translational Medicine

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BackgroundMatrix metalloproteinases can promote invasion and metastasis, which are very frequent in renal cell carcinoma even at the time of diagnosis. Knowing the reversion-inducing cysteine-rich protein with Kazal motifs (RECK) as an inhibitor of matrix metalloproteinases and the extracellular matrix metalloproteinase inducer (EMMPRIN) protein as inducer, we aimed to determine their expression, localization and possible antagonistic action in the pathogenesis and progression of renal cell tumors in a retrospective study.MethodsTumor and adjacent normal tissues of 395 nephrectomized patients were immunostained for RECK and EMMPRIN on a tissue microarray.ResultsRECK strongly decreased in renal cell carcinoma compared to normal counterparts (Wilcoxon signed rank test, P < 0.001), and it discriminated tumor entities showing the highest expression in oncocytomas. EMMPRIN, however, could be significantly correlated to pT stage and Fuhrman grading (Spearman’s correlation coefficient rs = 0.289 and rs = 0.382, respectively). Higher expression of EMMPRIN was associated with decreased overall survival in Kaplan-Meier analysis (P < 0.001), and the EMMPRIN level could independently predict survival for cases without metastasis and involvement of lymph nodes. Decreased RECK expression was confirmed by Western blotting in tissue of eight normal/tumor matches of patients after radical nephrectomy, whereas the EMMPRIN pattern appeared to be heterogeneous.ConclusionsWe propose RECK down regulation in renal cell carcinoma to be an early event that facilitates tumor formation and progression. EMMPRIN, however, as a prognostic tumor marker, increases only when aggressiveness is proceeding and could add an additional step to invasive properties of renal cell carcinoma.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Renal cell neoplasias: reversion-inducing cysteine-rich protein with Kazal motifs discriminates tumor subtypes, while extracellular matrix metalloproteinase inducer indicates prognosis

Rabien

Stephan

Kilic

et al. 2013

Journal of Translational Medicine

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“…To characterize the mechanism by which miR‐221 promotes tumor metastasis, we searched for potential target genes of miR‐221 using two publicly available databases, TargetScan and miRanda. We were particularly interested in MMP inhibitor and tumor suppressor RECK because in addition to its anti‐invasive properties [15], its mRNA and protein expression are negatively correlated with survival in colorectal cancer [20]. Our analysis of the 3′ UTR sequence of RECK identified a possible binding site for miR‐221 (Fig.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‐221 promotes colorectal cancer cell invasion and metastasis by targeting RECK

Qin

Luo

2013

FEBS Letters

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a b s t r a c tMicroRNAs (miRNAs) have recently emerged as regulators of metastasis. We provide insight into the behavior of miR-221 in colorectal cancer (CRC) metastasis by showing that miR-221 is significantly upregulated in metastatic CRC cell lines and tissues. miR-221 overexpression enhances, whereas miR-221 depletion reduces CRC cell migration and invasion in vitro and metastasis in vivo. We identify RECK as a direct target of miR-221, reveal its expression to be inversely correlated with miR-221 in CRC samples and show that its re-introduction reverses miR-221-induced CRC invasiveness. Collectively, miR-221 is an oncogenic miRNA which may regulate CRC migration and invasion through targeting RECK.

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“…Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) gene expresses in all human normal tissues but is down-regulated in a variety of tumor tissues including liver cancer [1], gastric cancer [2] and colorectal cancer [3]. RECK protein blocks the tumor metastasis and invasion via negative regulation of matrix metalloproteinases (MMPs) [4].…”

Section: Introductionmentioning

confidence: 99%

Suppression of Non-Small Cell Lung Cancer Growth and Metastasis by a Novel Small Molecular Activator of RECK

Shen¹,

Bang-hua²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Reversion-inducing cysteine-rich protein with kazal motifs (RECK) is a novel tumor suppressor gene that is critical for regulating tumor cell invasion and metastasis. The expression of RECK is dramatically down-regulated in human cancers. Harmine, a tricyclic compound from Peganum harmala, has been shown to have potential anti-cancer activity. Methods: Cell proliferation assay (CCK-8 cell viability assay), cell cycle analysis (detection by flow cytometry), apoptosis staining assay (TUNEL staining), cell migration assay and invasion assay (transwell assay) were carried out to investigate the Harmine’s efficacy on non-small cell lung cancer (NSCLC) cells in vitro. A549-luciferase cell orthotropic transplantation xenograft mouse model was used to determine the effect of Harmine treatment on NSCLC in vivo. Western blotting analysis of cell growth and metastasis related signal pathways was conducted to investigate the molecular mechanism of Harmine’s inhibitory effect on NSCLC. Results: Harmine treatment effectively inhibited cell proliferation and induced the G1/S cell cycle arrest of NSCLC cells. Further study proved that Harmine treatment led to apoptosis induction. Furthermore, treatment with NSCLC cells with Hamine resulted in decreased cell migration and cell invasion in vitro. More importantly, Harmine treatment significantly suppressed the NSCLC tumor growth and metastasis in mouse xenograft model in vivo. Mechanistically, in Harmine-treated NSCLC cells, RECK expression and its downstream signaling cascade were dramatically activated. As a consequence, the expression level of MMP-9 and E-cadherin were significantly decreased. Conclusion: These findings identify Harmine as a promising activator of RECK signaling for metastatic NSCLC treatment.

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Reversion-inducing cysteine-rich protein with Kazal motif (RECK) expression: an independent prognostic marker of survival in colorectal cancer

Cited by 18 publications

References 33 publications

Renal cell neoplasias: reversion-inducing cysteine-rich protein with Kazal motifs discriminates tumor subtypes, while extracellular matrix metalloproteinase inducer indicates prognosis

Renal cell neoplasias: reversion-inducing cysteine-rich protein with Kazal motifs discriminates tumor subtypes, while extracellular matrix metalloproteinase inducer indicates prognosis

MicroRNA‐221 promotes colorectal cancer cell invasion and metastasis by targeting RECK

Suppression of Non-Small Cell Lung Cancer Growth and Metastasis by a Novel Small Molecular Activator of RECK

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