Regulation of Epidermal Growth Factor Receptor Signaling in Human Cancer Cells by MicroRNA-7

Webster, Rebecca; Giles, Keith M.; Price, Karina J.; Zhang, Priscilla M; Mattick, John S.; Leedman, Peter J.

doi:10.1074/jbc.m804280200

Cited by 402 publications

(363 citation statements)

References 48 publications

(47 reference statements)

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“…It has been reported that miR-7 has a tumorsuppressor role in various cancers including brain tumors, breast cancer and lung cancer (Kefas et al, 2008;Reddy et al, 2008;Webster et al, 2009), and we herein showed that miR-7 also functions as a tumor suppressor in gastric cancer. Interestingly, in the normal stomach, miR-7 expression is induced during the differentiation of gastric epithelial cells, suggesting a role of miR-7 in the regulation of epithelial cell differentiation.…”

Section: Discussionsupporting

confidence: 66%

“…We found the expression level of miR-7 to significantly decrease in gastric tumors in an inflammation-dependent manner. It has been shown that miR-7 has a tumor-suppressor role in several cancers, including glioblastoma, breast cancer and lung cancer (Kefas et al, 2008;Reddy et al, 2008;Webster et al, 2009;Jiang et al, 2010;Saydam et al, 2011). In this manuscript, we demonstrate that miR-7 is induced during the differentiation of normal gastric epithelial cells, and it also has a tumor-suppressor role in the stomach.…”

supporting

confidence: 50%

“…The epidermal growth factor receptor (EGFR) mRNA is one of the miR-7 target genes (Kefas et al, 2008; Repression of miR-7 by inflammation D Kong et al Webster et al, 2009). We thus examined EGFR expression levels in pre-miR-7-transfected Kato-III and AZ521 gastric cancer cells.…”

Section: Inflammation-dependent Upregulation Of Mir-7 Target Genes Inmentioning

confidence: 99%

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Inflammation-induced repression of tumor suppressor miR-7 in gastric tumor cells

Kong

Piao

Yamashita³

et al. 2011

Oncogene

102

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Inflammation has an important role in cancer development through various mechanisms. It has been shown that dysregulation of microRNAs (miRNAs) that function as oncogenes or tumor suppressors contributes to tumorigenesis. However, the relationship between inflammation and cancer-related miRNA expression in tumorigenesis has not yet been fully understood. Using K19-C2mE and Gan mouse models that develop gastritis and gastritis-associated tumors, respectively, we found that 21 miRNAs were upregulated, and that 29 miRNAs were downregulated in gastric tumors in an inflammation-dependent manner. Among these miRNAs, the expression of miR-7, a possible tumor suppressor, significantly decreased in both gastritis and gastric tumors. Moreover, the expression of miR-7 in human gastric cancer was inversely correlated with the levels of interleukin-1b and tumor necrosis factor-a, suggesting that miR-7 downregulation is related to the severity of inflammatory responses. In the normal mouse stomach, miR-7 expression was at a basal level in undifferentiated gastric epithelial cells, and was induced during differentiation. Moreover, transfection of a miR-7 precursor into gastric cancer cells suppressed cell proliferation and soft agar colony formation. These results suggest that suppression of miR-7 expression is important for maintaining the undifferentiated status of gastric epithelial cells, and thus contributes to gastric tumorigenesis. Although epigenetic changes were not found in the CpG islands around miR-7-1 of gastritis and gastric tumor cells, we found that activated macrophage-derived small molecule(s) (o3 kDa) are responsible for miR-7 repression in gastric cancer cells. Furthermore, the miR-7 expression level significantly decreased in the inflamed gastric mucosa of Helicobacter-infected mice, whereas it increased in the stomach of germfree K19-C2mE and Gan mice wherein inflammatory responses were suppressed.Taken together, these results indicate that downregulation of tumor suppressor miR-7 is a novel mechanism by which the inflammatory response promotes gastric tumorigenesis.

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Section: Discussionsupporting

confidence: 66%

supporting

confidence: 50%

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Inflammation-induced repression of tumor suppressor miR-7 in gastric tumor cells

Kong

Piao

Yamashita³

et al. 2011

Oncogene

102

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“…27 Recent studies demonstrated that EGFR may be a functional target of miRNAs. 28,29 MiRNA-128, which is frequently deleted in lung cancers, directly downregulated EGFR, but did not correlate with EGFR mutation and prognosis. Overall, all these studies suggest that miRNAs can be used as diagnostic and prognostic markers of lung cancer.…”

mentioning

confidence: 90%

miRNA expression profiling of lung adenocarcinomas: correlation with mutational status

et al. 2010

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MicroRNA (miRNA) expression is deregulated in lung cancer, and some miRNAs are associated with poor prognosis and survival. In this study, we investigated the miRNA expression in lung adenocarcinomas with different oncogenic mutations, including EGFR-positive, KRAS-positive and EGFR/KRAS-negative tumors. The expression of 319 miRNAs was evaluated by Exiqon/Luminex microarray, and expression of individual miRNAs was validated by individual RT-PCR assays (Applied Biosystems). Overall, miRNA expression was similar among three mutationally different groups with most upregulated miRNAs being miR-20a, miR-328, miR-34c and miR-18b and most downregulated miRNAs being miR-32, miR-137 and miR-342. Four miRNAs (miR-155, miR-25, miR-495 and miR-7g) were expressed differently among these tumors. miR-155 was upregulated only in EGFR/KRAS-negative group, miR-25 was upregulated only in EGFR-positive group and miR-495 was upregulated only in KRAS-positive adenocarcinomas. In opposite, let-7g was downregulated in all three groups, with more significant downregulation in EGFR/KRASnegative adenocarcinomas. Principal component analysis (PCA) revealed significant correlation between miRNA expression patterns and somatic mutations. In this study, we demonstrated that despite the similarity in miRNA expression among lung adenocarcinomas with different somatic mutations, some miRNAs showed unique expression patterns, which were in strong correlation with the mutation type, suggesting different carcinogenic pathway for these tumors. These miRNAs can be further explored for their diagnostic and prognostic use.

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“…In addition, it still positively regulates miR-7 (Reddy et al, 2008), which was found to control epidermal growth factor receptor signaling and promote photoreceptor differentiation, inducing cell cycle arrest and cell death in some cancer cell lines (Kefas et al, 2008;Webster et al, 2009). miRNA expression profiling revealed that miR-7 was involved in tumor aggressiveness, invasion and metastasis in urothelial carcinomas and breast cancer (Foekens et al, 2008;Veerla et al, 2009).…”

Section: Pro-metastatic Mirnas Regulate Tumor Metastasismentioning

confidence: 99%

The microRNA network and tumor metastasis

2009

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Metastasis is the most significant process affecting the clinical management of cancer patients and occurs in multiple sequential steps. However, the molecular pathways underlying each step still remain obscure. Recent research has shown that there is a microRNA (miRNA) network that functions as a regulator of tumor metastasis. In this paper, we review the role of miRNAs in tumor metastasis, including control of epithelial-mesenchymal transition, regulation of metastasis-associated genes and epigenetic alterations. More information on miRNAs will promote a better understanding of the molecular mechanism of metastasis.

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Regulation of Epidermal Growth Factor Receptor Signaling in Human Cancer Cells by MicroRNA-7

Cited by 402 publications

References 48 publications

Inflammation-induced repression of tumor suppressor miR-7 in gastric tumor cells

Inflammation-induced repression of tumor suppressor miR-7 in gastric tumor cells

miRNA expression profiling of lung adenocarcinomas: correlation with mutational status

The microRNA network and tumor metastasis

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