MicroRNA‐1204 promotes cell proliferation by regulating PITX1 in non‐small‐cell lung cancer

Jiang, Wei; He, Yunjie; Shi, Yijun; Guo, Zizhang; Yang, Shuguang; Wei, Ke; Pan, Chunfeng; Xia, Yang; Chen, Yijiang

doi:10.1002/cbin.11083

Cited by 23 publications

(22 citation statements)

References 34 publications

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“…Both PVT1 and the well-known protein-coding gene MYC are co-located on the 8q24 chromosomal region, known as the gene desert, which contains a large number of risk alleles that are implicated in cancer [ 11 , 12 ]. PVT1 produces a wide variety of spliced non-coding RNAs, as well as a cluster of six annotated microRNAs: miR-1204, miR-1205, miR-1206, miR-1207-5p, miR-1207-3p, and miR-1208 [ 13 ], which can promote tumor proliferation [ 14 , 15 ], and the resistance of chemotherapy [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

Song

Pizzi

et al. 2020

Cancers

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Gastric adenocarcinoma (GAC) is inherently resistant or becomes resistant to therapy, leading to a poor prognosis. Mounting evidence suggests that lncRNAs can be used as predictive markers and therapeutic targets in the right context. In this study, we determined the role of lncRNA-PVT1 in GAC along with the value of inhibition of PVT1 using antisense oligos (ASOs). RNA scope in situ hybridization was used to analyze PVT1 expression in tumor tissue microarrays (TMAs) of GAC and paired normal tissues from 792 patients. Functional experiments, including colony formation and invasion assays, were performed to evaluate the effects of PVT1 ASO inhibition of PVT1 in vitro; patient-derived xenograft models were used to evaluate the anti-tumor effects of PVT1 ASOs in vivo. LncRNA-PVT1 was upregulated in GACs compared to the matched adjacent normal tissues in the TMA. LncRNA PVT1 expression was positively correlated with larger tumor size, deeper wall invasion, lymph node metastases, and short survival duration. Inhibition of PVT1 using PVT1 ASOs significantly suppressed tumor cell growth and invasion in vitro and in vivo. PVT1 expression was highly associated with poor prognosis in GAC patients and targeting PVT1 using PVT1 ASOs was effective at curtailing tumor cell growth in vitro and in vivo. Thus, PVT1 is a poor prognosticator as well as therapeutic target. Targeting PVT1 using PVT1 ASOs provides a novel therapeutic strategy for GAC.

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Section: Introductionmentioning

confidence: 99%

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

Song

Pizzi

et al. 2020

Cancers

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“…miR-1204 is a member of the PVT1 region. Recent studies have found that miR-1204 may improve B cell differentiation and metastasis in breast cancer and can target PITX1 in non-small cell lung cancer, which may be a poor prognostic factor and a potential therapeutic target for NSCLC [26]. We used three miRNA target prediction databases (miRanda, TargetScan, and miRWalk) to determine the target gene of miR-1204.…”

Section: Discussionmentioning

confidence: 99%

“…Alterations of the apoptosis play a significant role in the survival of abnormal cells and tumorigenesis [28,29]. Cell apoptosis is characterized by chromatin concentration, DNA fragmentation, membrane foaming, and/or apoptotic bodies [25][26][27][28][29][30]. In our study, Annexin V FITC analysis of flow cytometry and in vitro Hochest 33258 staining analysis indicated that the apoptosis rate of A549 and SPC cells in miR-1204 overexpression group was increased, while the apoptosis rate was found to have decreased in the miR-1204 inhibited group.…”

Section: Discussionmentioning

confidence: 99%

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The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK

Qian

Yang

Liu

et al. 2019

Folia Histochem Cytobiol.

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Introduction. This study endeavors to analyze the effects of miR-1204 on the expression of DEK oncogene in non-small cell lung cancer (NSCLC) cell lines and to study the molecular mechanisms of these effects. Material and methods. The miR-1204 mimics and inhibitors were transfected into the (A549 and SPC) NSCLC cells. Then the mRNA levels, cell viability, apoptosis rate, morphology and caspase activity were determined. The expression of apoptosis-related proteins Bcl-2 and Bax was also analyzed. Results. In NSCLC cell lines (A549 and SPC), DEK mRNA levels were down-regulated in miR-1204 overexpression group. In miR-1204 inhibition group, the expression of DEK mRNA showed an opposite trend. The overexpression of miR-1204 increases the apoptosis rate in NSCLC cells. The Bcl-2 level in the miR-1204 overexpression group was decreased, while the Bax level was increased. In the miR-1204 inhibition group, expression of Bcl-2 and Bax showed opposite trends. Cell staining revealed cell's morphological changes; the apoptosis in the miR-1204 overexpression group revealed significant morphological features, such as brighter nuclei and nuclear condensation. Results indicated a typical characteristic of apoptosis in the miR-1204 overexpression group. Caspase-9 and Caspase-3 were involved in the apoptosis pathway, which was mediated by miR-1204 and DEK. Conclusions. The miR-1204 induces apoptosis of NSCLC cells by inhibiting the expression of DEK. The mechanism of apoptosis involves down-regulation of Bcl-2 and up-regulation of Bax expression. Moreover, the apoptosis was mediated by mitochondria-related caspase 9/3 pathway.

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“…MiR-1204 facilitates the development of hepatocellular carcinoma by stimulating MAPK and c-JUN/AP1 pathway via targeting ZNF418 [26]. MiR-1204 induces the proliferation of non-smallcell lung cancer cells through modulating PITX1 expression [27]. However, the specific role of miR-1204 in GBM remains unclear, thus arousing our interest in exploring whether and how miR-1204 regulates the biological process in GBM cells, including cell proliferation and cell apoptosis.…”

Section: Introductionmentioning

confidence: 99%

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

Zhao¹,

Shen²,

Ma³

et al. 2020

Cancer Cell Int

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Background: Glioblastoma (GBM) is a subclass of brain malignancy with unsatisfactory prognosis. MicroRNAs (miR-NAs) are a group of non-coding RNAs (ncRNAs) that exert key function on tumorigenesis and tumor development. Purposes: The purpose of this work was to unravel the biological behavior and mechanism of miR-1204 in GBM. Methods: Expressions of miR-1204, NR3C2 and CREB1 were detected by RT-qPCR and western blot. Proliferation and apoptosis of GBM cells were detected by CCK-8, colony formation, caspase-3 activity and TUNEL assays. Molecular interplays were examined by ChIP, RIP, and luciferase reporter assays. Results: MiR-1204 level was elevated in GBM cell lines. Functionally, miR-1204 aggravated cell proliferation whereas suppressed cell apoptosis in GBM cells. Mechanistically, cAMP Responsive Element Binding Protein 1 (CREB1) bound to the promoter of miR-1204 and activated the transcription of miR-1204. Furthermore, miR-1204 targeted and inhibited Nuclear receptor subfamily 3 group C member 2 (NR3C2), a tumor suppressor gene in GBM cells. Rescue assays indicated that NR3C2 participated in the regulation of miR-1204 on the malignant phenotype of GBM cells. Conclusions: We observed for the first time that CREB1-induced miR-1204 promoted malignant phenotype of GBM through targeting NR3C2, indicating that miR-1204 acted as a novel oncogenic miRNA in GBM.

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MicroRNA‐1204 promotes cell proliferation by regulating PITX1 in non‐small‐cell lung cancer

Cited by 23 publications

References 34 publications

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

The miR-1204 regulates apoptosis in NSCLC cells by targeting DEK

CREB1-induced miR-1204 promoted malignant phenotype of glioblastoma through targeting NR3C2

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