Down-regulation of miR-31 expression in gastric cancer tissues and its clinical significance

Zhang, Yuanyuan; Guo, Junming; Li, Dong; Xiao, Bingxiu; Miao, Ying; Jiang, Zhen; Zhuo, Hui

doi:10.1007/s12032-009-9269-x

Cited by 95 publications

(62 citation statements)

References 22 publications

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“…Controlling expression of Radixin, miR-31 causes anoikis-mediated cell death. In agreement with these data, miR-31 expression has been found to be attenuated in human breast [88][89][90], prostate [91], ovary [92], stomach [93,94] and bladder cancer [95]. Moreover miR-31 levels in primary human breast tumors were inversely associated with distant metastases [86].…”

Section: Mirnas and Metastasissupporting

confidence: 71%

microRNA: New Players in Metastatic Process

Triulzi¹,

Iorio²,

Tagliabue³

et al. 2013

Oncogene and Cancer - From Bench to Clinic

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Section: Mirnas and Metastasissupporting

confidence: 71%

microRNA: New Players in Metastatic Process

Triulzi¹,

Iorio²,

Tagliabue³

et al. 2013

Oncogene and Cancer - From Bench to Clinic

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“…Association of miR-31 loss with the 9p21.3 lesion in cancer may have widespread clinical implications. Deletions that may potentially contain MIR31 have been recently reported in urothelial carcinomas (37), and down-regulation of this microRNA has been observed in gastric cancer (38). Also, 9p21.3 deletions were found in 31% of non-small lung cancers (39), ϳ85% of pancreatic adenocarcinomas (40), 35% of biliary tract tumors (41), 37.5% of osteosarcomas (42), 38% of soft tissue sarcomas (43), 75% of gliomas (44), 33-39% of T-cell acute lymphoblastic leukemias, 67% of primary cutaneous diffuse large B-cell lymphoma of the leg type (45), and ϳ17% of breast cancers (46).…”

Section: Discussionmentioning

confidence: 96%

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

Ivanov

Goparaju

Lopez

et al. 2010

Journal of Biological Chemistry

120

113

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The human genome encodes several hundred microRNA (miRNA) genes that produce small (21-23n) single strand regulatory RNA molecules. Although abnormal expression of miRNAs has been linked to cancer progression, the mechanisms of this dysregulation are poorly understood. Malignant mesothelioma (MM) of pleura is an aggressive and highly lethal cancer resistant to conventional therapies. We and others previously linked loss of the 9p21.3 chromosome in MM with short time to tumor recurrence. In this study, we report that MM cell lines derived from patients with more aggressive disease fail to express miR-31, a microRNA recently linked with suppression of breast cancer metastases. We further demonstrate that this loss is due to homozygous deletion of the miR-31-encoding gene that resides in 9p21.3. Functional assessment of miR-31 activity revealed its ability to inhibit proliferation, migration, invasion, and clonogenicity of MM cells. Re-introduction of miR-31 suppressed the cell cycle and inhibited expression of multiple factors involved in cooperative maintenance of DNA replication and cell cycle progression, including pro-survival phosphatase PPP6C, which was previously associated with chemotherapy and radiation therapy resistance, and maintenance of chromosomal stability. PPP6C, whose mRNA is distinguished with three miR-31-binding sites in its 3-untranslated region, was consistently down-regulated by miR-31 introduction and upregulated in clinical MM specimens as compared with matched normal tissues. Taken together, our data suggest that tumorsuppressive propensity of miR-31 can be used for development of new therapies against mesothelioma and other cancers that show loss of the 9p21.3 chromosome.

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“…For the detection of mature, single-stranded form of let-7a was performed using a miScript PCR system (Qiagen): miScript II RT Kit and miScript SYBR Green PCR Kit (26).…”

Section: Real-time Pcr Of Mirnasmentioning

confidence: 99%

The Downregulation of microRNA let-7a Contributes to the Excessive Expression of Type I Collagen in Systemic and Localized Scleroderma

Makino

Jinnin

Hirano

et al. 2013

The Journal of Immunology

146

111

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Systemic and localized scleroderma (SSc and LSc) is characterized by excessive deposition of collagen and tissue fibrosis in the skin. Although they have fundamental common characteristics including autoimmunity, little is known about the exact mechanism that mediates the excessive collagen expression in these disorders. In the current study, we tried to evaluate the possibility that microRNAs (miRNAs) play some roles in the pathogenesis of fibrosis seen in these diseases. miRNA expression patterns were evaluated by miRNA array analysis, real-time PCR, and in situ hybridization. The function of miRNAs in dermal fibroblasts was assessed using miRNA inhibitors, precursors, or protectors. In the mouse model of bleomycin-induced dermal sclerosis, the overexpression of miRNAs was performed by i.p. miRNA injection. We demonstrated let-7a expression was downregulated in SSc and LSc skin both in vivo and in vitro, compared with normal or keloid skin. The inhibition or overexpression of let-7a in human or mouse skin fibroblasts affected the protein expression of type I collagen or luciferase activity of collagen 3′-untranslated region. Also, we found let-7a was detectable and quantitative in the serum and investigated serum let-7a levels in patients with SSc or LSc. let-7a concentration was significantly decreased in these patients, especially in LSc patients. Moreover, we revealed that the intermittent overexpression of let-7a in the skin by i.p. miRNA injection improved the skin fibrosis induced by bleomycin in mice. Investigation of more detailed mechanisms of miRNA-mediated regulation of collagen expression may lead to new therapeutic approaches against SSc and LSc.

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Down-regulation of miR-31 expression in gastric cancer tissues and its clinical significance

Cited by 95 publications

References 22 publications

microRNA: New Players in Metastatic Process

microRNA: New Players in Metastatic Process

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

The Downregulation of microRNA let-7a Contributes to the Excessive Expression of Type I Collagen in Systemic and Localized Scleroderma

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