Long noncoding RNA RHPN1-AS1 promotes colorectal cancer progression via targeting miR-7-5p/OGT axis

Zheng, Wei; Li, Hui; Zhang, Hui; Zhang, Chao; Zhu, Zhongqi; Hong, Liang; Zhou, Yifeng

doi:10.1186/s12935-020-1110-9

Cited by 24 publications

(20 citation statements)

References 34 publications

(31 reference statements)

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“…For instance, a novel lncRNA LSAMP-AS1 is involved in PCa process via targeting miR-183-5p/DCN axis [8]. LncRNA RHPN1-AS1 has been claimed to accelerate the breast cancer development [9]. UCA1/miR-495/PRL-3 axis results in cell proliferation in gastric cancer [10].…”

Section: Introductionmentioning

confidence: 99%

LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

Ma¹,

Wang

Li³

et al. 2020

Cancer Cell Int

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Background Prostate cancer (PCa) is a kind of malignancy occurring in the prostate gland. Substantial researches have proved the major role of long noncoding RNAs (lncRNAs) in PCa. However, the role of long intergenic non-protein coding RNA 1006 (LINC01006) in PCa has not been investigated yet. Methods RT-qPCR was used to examine the expression levels of LINC01006 and its downstream targets. The function of LINC01006 in PCa was tested by in vitro and in vivo assays. With application of RNA pull down, RNA immunoprecipitation (RIP) and luciferase reporter assays, the interaction among LINC01006, miR-34a-5p and disheveled associated activator of morphogenesis 1 (DAAM1) were verified. Results LINC01006 expression presented high in PCa cell lines. LINC01006 silencing suppressed cell proliferative, migratory, invasive capacities while accelerated apoptotic rate. Besides, LINC01006 knockdown also suppressed tumor growth and metastasis in vivo. Furthermore, miR-34a-5p, a tumor suppressor in PCa, was sponged by LINC01006. Moreover, DAAM1 was targeted by miR-34a-5p and promoted PCa progression. More intriguingly, rescue assays suggested that the inhibitory effect of LINC01006 knockdown on PCa development was offset by DAAM1 overexpression. Conclusions LINC01006 promoted PCa progression by sponging miR-34a-5p to up-regulate DAAM1, providing a novel target for PCa therapy.

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Section: Introductionmentioning

confidence: 99%

LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

Ma¹,

Wang

Li³

et al. 2020

Cancer Cell Int

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“…lncRNA CASC9 expression was increased in primary colorectal cancer samples, and CASC9 initiates CRC development by regulating miR‐193a‐5p/ERBB2 axis 34 . lncRNA RHPN1‐AS1 was upregulated, and further RHPN1‐AS1 could indirectly regulate OGT through sponging miR‐7‐5p and then promote CRC cell proliferation and invasion 35 . Several studies have proved that MAGI2‐AS3 exerts an anti‐oncogenic effect in progression of human gliomas, 36 hepatocellular carcinoma cell, 25 and breast cancer 24 .…”

Section: Discussionmentioning

confidence: 99%

MAGI2‐AS3 rs7783388 polymorphism contributes to colorectal cancer risk through altering the binding affinity of the transcription factor GR to the MAGI2‐AS3 promoter

Yang

et al. 2020

Clinical Laboratory Analysis

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Background It has been indicated that the single nuclear polymorphisms (SNPs) in the long noncoding RNA (lncRNA) have association with colorectal cancer (CRC) susceptibility. Methods We enrolled 1078 cases with CRC and 1175 age‐ and gender‐matched cancer‐free controls to explore whether the polymorphisms in MAGI2‐AS3 have associations with CRC risk. qRT‐PCR, expression quantitative trait loci (eQTL) analyses, dual‐luciferase reporter assay, chromatin immunoprecipitation (ChIP), flow cytometry, and transwell assays were performed to explore the specific mechanisms in which MAGI2‐AS3 rs7783388 variation influenced the tumorigenesis of CRC. Results Subjects carrying rs7783388 GG genotype presented a higher risk of CRC compared with the AG/AA genotypes. Mechanistically, we found that the functional genetic variant of rs7783388 A > G decreased binding affinity of transcription factor glucocorticoid receptor (GR) to the MAGI2‐AS3 promoter, resulting in decreased transcriptional activity that subsequently downregulated MAGI2‐AS3 expression. Furthermore, functional experiments elucidated that MAGI2‐AS3 overexpression suppressed CRC cell proliferation, migration, and invasion capacities, arrested cell cycle at G0/G1 phase, and promoted cell apoptosis. Conclusion Taken together, our study demonstrated that the potential function of MAGI2‐AS3 as a tumor suppressor for CRC, and the MAGI2‐AS3 rs7783388 polymorphism is associated with the increased susceptibility to CRC by altering the binding ability of GR to the MAGI2‐AS3 promoter.

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“…In CRC, the abnormal expression of lncRNAs is crucial in regulating the multiplication, metastasis, apoptosis and other malignant biological behaviors of tumor cells 9 . For example, dysregulation of lncRNA CASC9, lncRNA HNF1A‐AS1 and lncRNA RHPN1‐AS1 is vital in the multiplication and metastasis of CRC 10–12 . According to previous studies, lncRNA MCM3AP antisense RNA 1 (lncRNA MCM3AP‐AS1) can regulate tumor progression in pancreatic cancer, glioblastoma and hepatocellular carcinoma 13–15 .…”

Section: Introductionmentioning

confidence: 99%

“…9 For example, dysregulation of lncRNA CASC9, lncRNA HNF1A-AS1 and lncRNA RHPN1-AS1 is vital in the multiplication and metastasis of CRC. [10][11][12] According to previous studies, lncRNA MCM3AP antisense RNA 1 (lncRNA MCM3AP-AS1) can regulate tumor progression in pancreatic cancer, glioblastoma and hepatocellular carcinoma. [13][14][15] However, the role and regulatory mechanism of MCM3AP-AS1 in CRC remain unclear.…”

mentioning

confidence: 99%

lncRNA MCM3AP‐AS1 inhibits the progression of colorectal cancer via the miR‐19a‐3p/FOXF2 axis

Dai

Zeng

Lee

2021

The Journal of Gene Medicine

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Background Long non‐coding RNA MCM3AP antisense RNA 1 (lncRNA MCM3AP‐AS1) has a regulatory role in the development of diverse malignancies, whereas its role and mechanism in colorectal cancer (CRC) is not yet clear. Methods The relative expression of MCM3AP‐AS1, miR‐19a‐3p and forkhead box F2 (FOXF2) mRNA in 53 cases of CRC and its adjacent normal tissues, human normal colonic mucosal cells (FHC cells) and CRC cell lines was examined by a quantitative real‐time polymerase chain reaction, and the changes of cell multiplication and migration were examined by the cell counting kit‐8 method, EdU test, and scratch‐healing test, respectively. Bioinformatics, dual‐luciferase reporter gene assay and a RNA immunoprecipitation experiment were adopted to predict and verify the relationship between MCM3AP‐AS1 and miR‐19a‐3p; bioinformatics and dual‐luciferase reporter gene assay were adopted to predict and verify the relationship between miR‐19a‐3p and FOXF2. Western blotting was executed to examine the effects of MCM3AP‐AS1 overexpression or knockdown on FOXF2 protein expression. Results MCM3AP‐AS1 expression was down‐modulated in CRC, and its dysregulation was linked to unfavorable pathological characteristics. MCM3AP‐AS1 significantly impeded the multiplication and migration of CRC cells. MCM3AP‐AS1 was recognized as a molecular sponge to suppress miR‐19a‐3p expression, and FOXF2 was a target gene of miR‐19a‐3p. MCM3AP‐AS1 positively modulated FOXF2 expression, and its biological effect was dependent the on miR‐19a‐3p/FOXF2 axis. Conclusions MCM3AP‐AS1 can inhibit CRC promoting by modulating the miR‐19a‐3p/FOXF2 axis.

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Long noncoding RNA RHPN1-AS1 promotes colorectal cancer progression via targeting miR-7-5p/OGT axis

Cited by 24 publications

References 34 publications

LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1

MAGI2‐AS3 rs7783388 polymorphism contributes to colorectal cancer risk through altering the binding affinity of the transcription factor GR to the MAGI2‐AS3 promoter

lncRNA MCM3AP‐AS1 inhibits the progression of colorectal cancer via the miR‐19a‐3p/FOXF2 axis

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