MiR-218 Mediates tumorigenesis and metastasis: Perspectives and implications

Lu, Yuan-Qiang; Zhang, Li; Waye, Mary Miu Yee; Fu, Weiming; Zhang, Jinfang

doi:10.1016/j.yexcr.2015.03.027

Cited by 50 publications

(44 citation statements)

References 76 publications

(139 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miR-218 suppresses cancer progression by targeting the mRNAs encoding survivin (17), HOXB3 (29), Bmi1 (30), and components of the AKT/mTOR, SLIT/ROBO, wnt, and focal adhesion pathways (15). In this study, we found that expression of miR-218-1 and miR-218-2 correlated negatively with CpG island methylation in SLIT2 and SLIT3, respectively (Fig.…”

Section: Discussionmentioning

confidence: 52%

“…The expression of miR-218 is significantly repressed in gastric, colon, prostate, and pancreatic cancers (15). miR-218 suppresses cancer progression by targeting the mRNAs encoding survivin (17), HOXB3 (29), Bmi1 (30), and components of the AKT/mTOR, SLIT/ROBO, wnt, and focal adhesion pathways (15).…”

Section: Discussionmentioning

confidence: 99%

“…miR-218 is the mature form of miR-218-1 and miR218-2, the intronic miRNAs that share the same promoter with their host gene transcripts, SLIT2 and SLIT3, respectively (15). miRNA-seq of patient-derived gastric cancer cells and adjacent normal gastric mucosa cells showed that expression of miR-218-1 and miR-218-2 was silenced in gastric cancer cells (Fig.…”

Section: Downregulation Of Mir-218 Through Methylation Of Slit2mentioning

confidence: 99%

“…miR-218 is an intronic microRNA (miRNA) co-expressed with its host genes, SLIT2 and SLIT3 (15). The mature form of miR-218 is generated from two separate loci, miR-128-1 and miR-218-2, which are located within the introns of SLIT2 and SLIT3, respectively (16).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

Kim

Baek

et al. 2016

International Journal of Oncology

View full text Add to dashboard Cite

Abstract. SLIT has been suggested as a key regulator of cancer development and a promising therapeutic target for cancer treatment. Herein, we analyzed expression and methylation of SLIT1/SLIT2/SLIT3 in 11 gastric cancer cell lines, 96 paired gastric tumors and adjacent normal gastric tissues, and 250 gastric cancers provided by The Cancer Genome Atlas. Methylation of SLIT1/SLIT2/SLIT3 was found both in early gastric cancers, and in advanced gastric cancers. Even normal gastric tissue showed increased methylation of SLIT1 and SLIT3 that correlated with patient age. Furthermore, epigenetic inactivation of SLIT occurred in a gastric cancer subtype-dependent manner. SLIT2 and SLIT3 expression was reduced in Epstein-Barr virus-positive and microsatellite instability subtypes, but increased in the genomically stable subtype. Expression of miR-218 correlated negatively with methylation of SLIT2 or SLIT3. These findings suggest that a molecular subtype-specific therapeutic strategy is needed for targeting SLITs and miR-218 in treatment of gastric cancer.

show abstract

Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Downregulation Of Mir-218 Through Methylation Of Slit2mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

Kim

Baek

et al. 2016

International Journal of Oncology

View full text Add to dashboard Cite

show abstract

“…Recent studies revealed that miR-218, as a tumor suppressor, was strongly downexpressed and related to proliferation, apoptosis and invasion in cervical cancer and some other cancers [16–19]. Some studies also demonstrated that the expression of miR-218 was strongly downregulated by HPV E6 [14, 20], but the mechanisms of the function of HPV on miR-218 and the role of miR-218 on the metastasis of cervical cancer are not well understood.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-218 inhibits EMT, migration and invasion by targeting SFMBT1 and DCUN1D1 in cervical cancer

et al. 2016

View full text Add to dashboard Cite

Repeated infection with high-risk HPV is a major cause for the development and metastasis of human cervical cancer, even though the mechanism of the metastasis is still not completely understood. Here, we reported that miR-218 (microRNA-218) was downregulated in cervical cancer tissues, especially in metastatic cancer tissues. We found that miR-218 expression was associated with clinicopathological characteristics of patients with cervical cancer. MiR-218 overexpression inhibited Epithelial-Mesenchymal Transition (EMT), migration and invasiveness of cervical cancer cells in vitro. Moreover, miR-218 repressed the expression of SFMFBT1 (Scm-like with four MBT domains 1) and DCUN1D1 (defective in cullin neddylation 1, domain containing 1) by direct binding to the 3′UTRs of the mRNAs. The overexpression of SFMBT1 induced EMT and increased the migration and invasiveness of cervical cancer cells, while the overexpression of DCUN1D1 increased the migration and invasiveness of these cells, but did not induce EMT. An inverse correlation was observed between the expression of miR-218 and DCUN1D1 protein in cervical cancer tissues. Importantly, HPV16 E6 downregulated the expression of miR-218 in cervical cancer, while miR-218 rescued the promotion effect of HPV16 E6 on the expression of SFMBT1 and DCUN1D1. Taken together, our results revealed that HPV16 E6 promoted EMT and invasion in cervical cancer via the repression of miR-218, while miR-218 inhibited EMT and invasion in cervical cancer by targeting SFMBT1 and DCUN1D1.

show abstract

Emerging Role of MicroRNAs in mTOR Signaling

Zhang

Huang

Wang³

et al. 2017

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Mechanistic target of rapamycin (mTOR) is a conserved serine/threonine kinase that plays a critical role in the control of cellular growth and metabolism. Hyperactivation of mTOR pathway is common in human cancers, driving uncontrolled proliferation. MicroRNA (miRNA) is a class of short noncoding RNAs that regulate the expression of a wide variety of genes. Deregulation of miRNAs is a hallmark of cancer. Recent studies have revealed interplays between miRNAs and the mTOR pathway during cancer development. Such interactions appear to provide a fine-tuning of various cellular functions and contribute qualitatively to the behavior of cancer. Here we provide an overview of current knowledge regarding the reciprocal relationship between miRNAs and mTOR pathway: regulation of mTOR signaling by miRNAs and control of miRNA biogenesis by mTOR. Further research in this area may prove important for the diagnosis and therapy of human cancer.

show abstract

MiR-218 Mediates tumorigenesis and metastasis: Perspectives and implications

Cited by 50 publications

References 76 publications

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

Specific expression and methylation of SLIT1, SLIT2, SLIT3, and miR-218 in gastric cancer subtypes

MicroRNA-218 inhibits EMT, migration and invasion by targeting SFMBT1 and DCUN1D1 in cervical cancer

Emerging Role of MicroRNAs in mTOR Signaling

Contact Info

Product

Resources

About