Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Xu, Jing; Wu, Guanghai; Zhao, Yan; Han, Youkui; Zhang, Shuai; Li, Chao; Zhang, Judong

doi:10.7150/jca.46562

Cited by 23 publications

(16 citation statements)

References 39 publications

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“…Another study in colorectal cancer cells has shown the sponging effect of DSCAM-AS1 on miR-137 ( Xu et al, 2020 ). This miRNA has been found to suppress expression of Notch-1, a protein with essential roles in cell proliferation and epithelial-mesenchymal transition (EMT) ( Chu et al, 2019 ).…”

Section: Cell Line Experimentsmentioning

confidence: 99%

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A Review on the Carcinogenic Roles of DSCAM-AS1

Ghafouri‐Fard

Khoshbakht

Taheri

et al. 2021

Front. Cell Dev. Biol.

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Long non-coding RNAs (lncRNAs) are a group of transcripts with fundamental roles in the carcinogenesis. DSCAM Antisense RNA 1 (DSCAM−AS1) is an example of this group of transcripts which has been firstly identified in an attempt to find differentially expressed transcripts between breast tumor cells and benign breast samples. The pathogenic roles of DSCAM-AS1 have been vastly assessed in breast cancer, yet its roles are not restricted to this type of cancer. Independent studies in non-small cell lung cancer, colorectal cancer, osteosarcoma, hepatocellular carcinoma, melanoma and cervical cancer have validated participation of DSCAM-AS1 in the carcinogenic processes. miR-577, miR-122-5p, miR-204-5p, miR-136, miR−137, miR−382, miR−183, miR−99, miR-3173-5p, miR-874-3p, miR-874-3p, miR-150-5p, miR-2467-3p, miR-216b, miR-384, miR-186-5p, miR-338-3p, miR-877-5p and miR-101 are among miRNAs which interact with DSCAM-AS1. Moreover, this lncRNA has interactions with Wnt/β-catenin pathway. The current study aims at summarization of the results of studies which focused on the assessment of oncogenic role of DSCAM-AS1.

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Section: Cell Line Experimentsmentioning

confidence: 99%

“…This miRNA has been found to suppress expression of Notch-1, a protein with essential roles in cell proliferation and epithelial-mesenchymal transition (EMT) ( Chu et al, 2019 ). Suppression of DSCAM-AS1 expression in colorectal cancer cells has resulted in down-regulation of Notch-1 ( Xu et al, 2020 ).…”

Section: Cell Line Experimentsmentioning

confidence: 99%

A Review on the Carcinogenic Roles of DSCAM-AS1

Ghafouri‐Fard

Khoshbakht

Taheri

et al. 2021

Front. Cell Dev. Biol.

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“…Bioinformatics analyses predicted the presence of a miR-137 seed region in the MSH2 3′UTR—with our in vitro results confirming MSH2 is targeted by miR-137. MiR-137, which is located on human chromosome 1p22, is reportedly present in neuronal cells [ 37 , 38 , 39 , 40 ], but is also found constitutively expressed in normal colonic epithelium [ 27 , 28 , 41 , 42 , 43 , 44 ], while low expression is found in adenomatous polyps and tumoral colorectal tissues [ 21 ]. Moreover, miR-137 locus is frequently hypermethylated in several tumor types, including colorectal, gastric, breast, head and neck squamous cell carcinoma, and colorectal adenomatous tissue [ 45 , 46 , 47 , 48 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-137 Targets the 3′ Untranslated Region of MSH2: Potential Implications in Lynch Syndrome-Related Colorectal Cancer

Liccardo

Sessa

Trombetti

et al. 2021

Cancers

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Mismatch Repair (MMR) gene dysregulation plays a fundamental role in Lynch Syndrome (LS) pathogenesis, a form of hereditary colorectal cancer. Loss or overexpression of key MMR genes leads to genome instability and tumorigenesis; however, the mechanisms controlling MMR gene expression are unknown. One such gene, MSH2, exerts an important role, not only in MMR, but also in cell proliferation, apoptosis, and cell cycle control. In this study, we explored the functions and underlying molecular mechanisms of increased MSH2 expression related to a c.*226A>G variant in the 3′untranslated (UTR) region of MSH2 that had been previously identified in a subject clinically suspected of LS. Bioinformatics identified a putative binding site for miR-137 in this region. To verify miRNA targeting specificity, we performed luciferase gene reporter assays using a MSH2 3′UTR psiCHECK-2 vector in human SW480 cells over-expressing miR-137, which showed a drastic reduction in luciferase activity (p > 0.0001). This effect was abolished by site-directed mutagenesis of the putative miR-137 seed site. Moreover, in these cells we observed that miR-137 levels were inversely correlated with MSH2 expression levels. These results were confirmed by results in normal and tumoral tissues from the patient carrying the 3′UTR c.*226A>G variant in MSH2. Finally, miR-137 overexpression in SW480 cells significantly suppressed cell proliferation in a time- and dose-dependent manner (p < 0.0001), supporting a role for MSH2 in apoptosis and cell proliferation processes. Our findings suggest miR-137 helps control MSH2 expression via its 3′UTR and that dysregulation of this mechanism appears to promote tumorigenesis in colon cells.

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“…LncRNA down syndrome cell adhesion molecule antisense RNA 1 (DSCAM-AS1) was originally identified as the most abundant Apo-ERα-regulated lncRNA (AER-lncRNA) in breast cancer [ 80 ]. Subsequent work ascribed an oncogenic role for DSCAM-AS1, with the expression in colorectal cancer associated with metastasis, advanced stage and poor overall survival [ 81 ], and in breast cancer linked with tumor progression and tamoxifen resistance [ 82 , 83 ]. Similarly, DSCAM-AS1 was proven highly expressed in osteosarcoma cell lines.…”

Section: Regulatory Network Of Lncrnas and Wnt Signaling Pathway In Osteosarcomamentioning

confidence: 99%

Functional interplay between long non-coding RNAs and the Wnt signaling cascade in osteosarcoma

Lin

Liu

et al. 2021

Cancer Cell Int

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Osteosarcoma is a common and highly malignant bone tumor among children, adolescents and young adults. However, the underlying molecular mechanisms remain largely unexplored. LncRNAs are transcripts with no or limited protein-coding capacity in human genomes, and have been demonstrated to play crucial functions in initiation, progression, therapeutic resistance, recurrence and metastasis of tumor. Considerable studies revealed a dysregulated lncRNA expression pattern in osteosarcoma, which may act as oncogenes or suppressors to regulate osteosarcoma progression. Wnt signaling pathway is an important cascade in tumorigenesis by modulation of pleiotropic biological functions including cell proliferation, apoptosis, differentiation, stemness, genetic stability and chemoresistance. Hyperactivation or deficiency of key effectors in Wnt cascade is a common event in many osteosarcoma patients. Recently, increasing evidences have suggested that lncRNAs could interplay with component of Wnt pathway, and thereby contribute to osteosarcoma onset, progression and dissemination. In this review, we briefly summarize Wnt signaling-related lncRNAs in osteosarcoma progression, aiming to gain insights into their underlying crosstalk as well as clinical application in osteosarcoma therapeutic modalities.

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Long Noncoding RNA DSCAM-AS1 Facilitates Colorectal Cancer Cell Proliferation and Migration via miR-137/Notch1 Axis

Cited by 23 publications

References 39 publications

A Review on the Carcinogenic Roles of DSCAM-AS1

A Review on the Carcinogenic Roles of DSCAM-AS1

MiR-137 Targets the 3′ Untranslated Region of MSH2: Potential Implications in Lynch Syndrome-Related Colorectal Cancer

Functional interplay between long non-coding RNAs and the Wnt signaling cascade in osteosarcoma

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