LncRNA PART1 regulates colorectal cancer via targeting miR-150-5p/miR-520h/CTNNB1 and activating Wnt/β-catenin pathway

Zhou, Taicheng; Wu, Lili; Ma, Ning; Tang, Fuxin; Zong, Zhen; Chen, Shuang

doi:10.1016/j.biocel.2019.105637

Cited by 49 publications

(26 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increasing evidence indicates that miRNAs might be sponged by lncRNAs to regulate disease-related gene expression, resulting in the regulation of disease progression. Hence, lncRNAs may serve as competitive endogenous RNAs (ceRNAs) (18). For example, miR-495-3p is sponged by lncRNA NEAT1 to regulate STAT3 expression, resulting in alleviation of septicemia-related inflammatory response (19).…”

Section: Introductionmentioning

confidence: 99%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

View full text Add to dashboard Cite

Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non-coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B-cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK-8, clone formation, wound-healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR-495-3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR-495-3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR-495-3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR-495-3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR-495-3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.

show abstract

Section: Introductionmentioning

confidence: 99%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…Previous reports have shown that PART1 acts as a ceRNA on seven miRNA targets; miR-635 [ 54 ], miR-129 [ 28 ], miR-373-3p [ 55 ], miR-429 [ 55 ], miR-150-5p [ 56 , 57 ], miR-143-3p [ 27 ], and miR-190a-3p [ 30 ]. We used TargetScan [ 55 ] to identify the predicted mRNA targets for each of these seven miRNAs.…”

Section: Resultsmentioning

confidence: 99%

“…In colorectal cancer, PART1 promotes tumor growth by acting as a ceRNA, sponging miR-143 [ 27 ]. Similarly, PART1 was shown to promote malignant progression of colorectal cancer through the miR-150-5p / LRG1 axis [ 56 ] and by sponging miR-150-5p to up-regulate the expression of CTNNB1 and activate Wnt/β-catenin signaling [ 57 ]. Conversely, PART1 has tumor suppressive function in glioma by sponging miR-190a-3p , leading to upregulation miR-190a-3p target PTEN (a tumor suppressor), which subsequently inactivates the PI3K/AKT pathway in glioma cell lines [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA PART1 Promotes Proliferation and Migration, Is Associated with Cancer Stem Cells, and Alters the miRNA Landscape in Triple-Negative Breast Cancer

Cruickshank

Wasson

Brown

et al. 2021

Cancers

View full text Add to dashboard Cite

Triple-negative breast cancers (TNBCs) are aggressive, lack targeted therapies and are enriched in cancer stem cells (CSCs). Novel therapies which target CSCs within these tumors would likely lead to improved outcomes for TNBC patients. Long non-coding RNAs (lncRNAs) are potential therapeutic targets for TNBC and CSCs. We demonstrate that lncRNA prostate androgen regulated transcript 1 (PART1) is enriched in TNBCs and in Aldefluorhigh CSCs, and is associated with worse outcomes among basal-like breast cancer patients. Although PART1 is androgen inducible in breast cancer cells, analysis of patient tumors indicates its androgen regulation has minimal clinical impact. Knockdown of PART1 in TNBC cell lines and a patient-derived xenograft decreased cell proliferation, migration, tumor growth, and mammosphere formation potential. Transcriptome analyses revealed that the lncRNA affects expression of hundreds of genes (e.g., myosin-Va, MYO5A; zinc fingers and homeoboxes protein 2, ZHX2). MiRNA 4.0 GeneChip and TaqMan assays identified multiple miRNAs that are regulated by cytoplasmic PART1, including miR-190a-3p, miR-937-5p, miR-22-5p, miR-30b-3p, and miR-6870-5p. We confirmed the novel interaction between PART1 and miR-937-5p. In general, miRNAs altered by PART1 were less abundant than PART1, potentially leading to cell line-specific effects in terms miRNA-PART1 interactions and gene regulation. Together, the altered miRNA landscape induced by PART1 explains most of the protein-coding gene regulation changes (e.g., MYO5A) induced by PART1 in TNBC.

show abstract

“…14,15 LncRNA PART1 regulated miR-150-5p/ miR-520h/CTNNB1 axis and activated wnt/β-catenin pathway in colorectal cancer. 16 In addition, wnt/β-catenin pathway was involved in glioma formation. 17 However, whether FGD5-AS1 interacts with wnt/β-catenin pathway in glioma remains elusive.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway</p>

Zhao¹,

Xue²,

Zhang³

et al. 2020

CMAR

View full text Add to dashboard Cite

Purpose: To investigate the specific function of long noncoding RNA FGD5 antisense RNA 1 (lncRNA FGD5-AS1) in glioma. Materials and Methods: The level of FGD5-AS1 was detected in clinical samples and cell lines by qRT-PCR. Small interfering RNA (siRNA) of FGD5-AS1 or scramble siRNA was transfected into U87 cell lines to examine the role of FGD5-AS1 on glioma development. The proliferation of glioma cells was tested by Cell Counting Kit-8 (CCK-8), the migration and invasion of glioma cells were tested by transwell assay without matrigel or with matrigel. Western blot was used to detect the protein expression, and XAV-939 was used to inhibit wnt/β-catenin pathway. The effect of FGD5-AS1 on tumorigenesis of glioma was confirmed by xenograft nude mice model. Results: FGD5-AS1 was significantly increased in glioma tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of U87 cells. Furthermore, overexpression of FGD5-AS1 increased the mRNA and protein levels of β-catenin and cyclin D1. Blocking of wnt/β-catenin using XAV-939 reversed the promotion role of FGD3-AS1 on glioma cells' migration and invasion. The in vivo tumor growth assay showed that FGD3-AS1 accelerated glioma tumorigenesis with activating wnt/β-catenin pathway. Conclusion: Our research emphasized FGD5-AS1 acting as an oncogene by regulating wnt/ β-catenin signaling pathway, thus providing some novel experimental basis for clinical treatment of glioma.

show abstract

LncRNA PART1 regulates colorectal cancer via targeting miR-150-5p/miR-520h/CTNNB1 and activating Wnt/β-catenin pathway

Cited by 49 publications

References 34 publications

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

LncRNA PART1 Promotes Proliferation and Migration, Is Associated with Cancer Stem Cells, and Alters the miRNA Landscape in Triple-Negative Breast Cancer

<p>Long Noncoding RNA FGD5-AS1 Promotes Glioma Cell Proliferation, Migration and Invasion by Regulating wnt/β-Catenin Pathway</p>

Contact Info

Product

Resources

About