Dataset Information

LINC00152 promotes pancreatic cancer cell proliferation, migration and invasion via targeting miR-150.

ABSTRACT: Pancreatic cancer (PC) is one of the top deaths causing cancers with low 5-year survival rate. Long non-coding RNAs (lncRNAs) are recognized as a crucial type of nonprotein-coding transcripts implicated in tumorigenesis. Emerging evidence has implied that LINC00152 exerts the potential oncogenic functions in various cancers. Nevertheless, the role of LINC00152 in PC remains elusive. In the present study, we found that LINC00152 was significantly up-regulated while miR-150 was down-regulated both in tissues and cell lines of PC, indicating their negative correlation in PC progression. Functionally, overexpression of LINC00152 promoted cell proliferation, migration and invasion, while LINC00152 knockdown reversed these effects. Mechanistic experiments reveal that miR-150 acted as a target of LINC00152 confirmed by luciferase reporter assay. Moreover, inhibition of miR-150 could markedly attenuate the suppression of cell proliferation, migration and invasion by knocking down LINC00152. Altogether, our findings concluded that LINC00152 facilitated PC progression through inhibiting miR-150 expression, indicating an innovative therapeutic target for PC.

SUBMITTER: Yuan ZJ

PROVIDER: S-EPMC7269995 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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LINC00152 promotes pancreatic cancer cell proliferation, migration and invasion via targeting miR-150.

Yuan Zhi-Jun ZJ Yu Can C Hu Xiao-Fang XF He Yi Y Chen Po P Ouyang Sha-Xi SX

American journal of translational research 20200515 5

Pancreatic cancer (PC) is one of the top deaths causing cancers with low 5-year survival rate. Long non-coding RNAs (lncRNAs) are recognized as a crucial type of nonprotein-coding transcripts implicated in tumorigenesis. Emerging evidence has implied that LINC00152 exerts the potential oncogenic functions in various cancers. Nevertheless, the role of LINC00152 in PC remains elusive. In the present study, we found that LINC00152 was significantly up-regulated while miR-150 was down-regulated both ...[more]

PMID: 32509216

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Project description:The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR-663b. It was demonstrated that miR-663b was significantly upregulated in NPC tissue compared with non-tumor nasopharyngeal epithelial tissue samples. Furthermore, miR-663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR-663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR-663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR-663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR-663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR-663b negatively regulated the expression of TUSC2 at the post-transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR-663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR-663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR-663b is a promising therapeutic target for the treatment of patients with NPC.

Dataset Information

LINC00152 promotes pancreatic cancer cell proliferation, migration and invasion via targeting miR-150.

Publications

LINC00152 promotes pancreatic cancer cell proliferation, migration and invasion via targeting miR-150.

Similar Datasets

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