DICER-AS1 functions as competing endogenous RNA that targets CSR1 by sponging microRNA-650 and suppresses gastric cancer progression

An, Junyan; Guo, Xiaoling; Yan, Bingli

doi:10.1177/03000605211041466

Cited by 2 publications

(3 citation statements)

References 25 publications

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“…Previously, Zhang et al [15] reported that overexpression of miR-650 promoted GC tumorigenesis in vivo and GC cell clonogenicity in vivo. Moreover, the overexpression of miR-650 has a positively association with the advancement of GC, as demonstrated in the work of Liu et al [46] and An et al [47].…”

Section: Mir-650 and Gastric Cancer (Gc)mentioning

confidence: 80%

“…It is worth mentioning that other researchers have found that constructed adenoviruses carrying the NDRG2 gene heightened p53-mediated apoptosis of HCC cells [66]. Moreover, CSR1 has also been reported to be a shared gene targeted Tumour volume, tumour metastasis, mortality of severe [63] Table 2 The roles of miR-650 in various cancer cell lines by miR-650 in both GC [47] and prostate cancer [63]. In addition to cell proliferation and apoptosis, overexpression of miR-650 induces EMT of cancer cells [11,14,30,49,67], which is a key factor in promoting the metastasis of tumours [68].…”

Section: Mir-650 Functions As a Tumour Promotermentioning

confidence: 97%

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Functions and underlying mechanisms of miR-650 in human cancers

Zheng

Zhu

et al. 2022

Cancer Cell Int

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MicroRNAs (miRNAs) are one type of noncoding RNAs that interfere with mRNA translation to downregulate gene expression, which results in posttranscriptional gene silencing. Over the past two decades, miRNAs have been widely reported to impact the progression of malignant tumours by interfering with cancer initiation and progression; therefore, miRNAs represent potential new diagnostic and therapeutic tools. miR-650 is a newly identified miR, and increasing studies have demonstrated that miR-650 plays critical roles in cancer progression, such as mediating the Wnt signalling pathway/AXIN1 (axis inhibition protein 1) axis in hepatocellular carcinoma. Nevertheless, associations between the expression patterns and molecular mechanisms of miR-650 in cancer have not been comprehensively described. In this article, we review the existing evidence regarding the mechanisms by which miR-650 expression is altered and their relation to cancer. Moreover, the promising clinical application of miR-650 for diagnosis and treatment is highlighted.

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Section: Mir-650 and Gastric Cancer (Gc)mentioning

confidence: 80%

Section: Mir-650 Functions As a Tumour Promotermentioning

confidence: 97%

Functions and underlying mechanisms of miR-650 in human cancers

Zheng

Zhu

et al. 2022

Cancer Cell Int

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“…DICER-AS1 acts as ceRNA to target CSR1 by sponging microRNA-650 to obstruct gastric cancer progression. 28 Still, miRNAs decrease the stability of lncRNAs. 29 A previous study reported that overexpression of let-7b facilitate the degradation of RNA, inducing the instability of lncRNA-p21.…”

Section: Discussionmentioning

confidence: 99%

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

Chen¹,

Liao²,

Xu³

et al. 2022

CMAR

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Background Long non-coding RNA LINC01232 plays an important role in the progression of metastasis in several cancers. However, the function of LINC01232 in gastric cancer is limited. Authors aimed to investigate the role and mechanism of LINC01232 in the metastasis of gastric cancer. Methods The expression levels and correlation of LINC01232, miR-506-5p, and PAK1 were analyzed by GEPIA or ENCORI, and the abundance of LINC01232 and miR-506-5p was measured in tissues and cells via qRT-PCR, the location of LINC01232 in gastric cells was analyzed by nuclear and cytoplasmic fractionation, while the protein levels of PAK1, E-cadherin and vimentin were additionally quantified by Western blotting. Interactions between LINC01232, miR-506-5p, and PAK1 were detected through luciferase reporter assays, qRT-PCR and Western blotting. Cellular viability was evaluated through CCK8 assays, migration ability was measured by transwell assays, invasion ability was tested by wound healing experiment. Results LINC01232 was overexpressed in gastric cancer tissues and cells, and mainly located in nucleus. The inhibition of LINC01232 could suppress migration, invasion and EMT of gastric cancer cells. MiR-506-5p was downregulated in gastric cancer tissues and cells. LINC01232 sponged miR-506-5p to accelerate migration and EMT. PAK1 was certified to be a target of miR-506-5p, inhibition of PAK1 could interrupt LINC01232 overexpression-induced migration of gastric cancer cells. Conclusion The LINC01232/miR-506-5p/PAK1 axis promotes metastasis of gastric cancer cells.

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DICER-AS1 functions as competing endogenous RNA that targets CSR1 by sponging microRNA-650 and suppresses gastric cancer progression

Cited by 2 publications

References 25 publications

Functions and underlying mechanisms of miR-650 in human cancers

Functions and underlying mechanisms of miR-650 in human cancers

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

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