Long intergenic non‑protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA‑497

Yu, Tianhua; Xu, Zhihua; Zhang, Xuanhe; Men, Lan; Nie, Haiying

doi:10.3892/or.2018.6721

Cited by 10 publications

(9 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Growing evidence has suggested that a number of lncRNAs contribute to the progression of MM, and can serve as effective diagnosis markers, and therapeutic targets for MM [9,10]. Yu et al [26] reported that long intergenic non-protein coding RNA 152 drove MM progression by negatively regulating miR-497. Shen et al [27] revealed that lncRNA MEG3 promoted MM progression by functioning as a ceRNA to regulate HOXA11 expression by sponging miR-181a.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

2019

View full text Add to dashboard Cite

Background: Long non-coding RNA taurine up-regulated gene 1 (TUG1) was reportedly involved in initiation and development of several cancers. However, its function and molecular mechanisms in multiple myeloma (MM) are still unclear. The present study aimed to determine the expression status, biological function, and potential mechanisms of TUG1 in the progression of MM. Materials and methods: The expression levels of TUG1 were examined in MM samples and cell lines by real-time quantitative PCR. The effects of TUG1 on MM cells proliferation and apoptosis were assessed using Cell Counting Kit-8 assay and flow cytometry respectively. MiRNAs-targeted sites in TUG1 were screened by Starbase2.0 and were identified by RNA immunoprecipitation assay combined with luciferase reporter assay. Results: The expression levels of TUG1 were markedly increased in MM samples and cell lines. Knockdown of TUG1 significantly suppressed the proliferation, induced cell cycle arrest at G1/G0 phase, and promoted apoptosis of MM cells. In exploring the regulatory mechanism, miR-29b-3p was confirmed to be a direct target of TUG1, and repression of miR-29b-3p could partially rescue the effect TUG1 knockdown on MM cell proliferation, cycle, and apoptosis. In addition, TUG1 positively modulated histone deacetylases 4 (HDAC4, a target of miR-29b-3p) expression through sponging of miR-29b-3p in MM cells. Conclusion: These findings suggested that TUG1 exerted an oncogenic role in MM by acting as a competing endogenous RNA of miR-29b-3p, and implied the potential application of TUG1 in treatment for MM.

show abstract

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

2019

View full text Add to dashboard Cite

show abstract

“…In thyroid cancer, LINC00152 acts as a miR-497 'sponge', downregulating its downstream target, brain-derived neurotrophic factor (BDNF), to promote the proliferation and invasion of papillary thyroid cancer cells (71). In multiple myeloma, LINC00152 acts as an oncogene and regulates cell growth by targeting miR-497 expression (72).…”

Section: Epigeneticsmentioning

confidence: 99%

Regulation of microRNA‑497 expression in human cancer (Review)

Luo

Xia

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

“…A recent publication also found LINC00152 to regulate proliferation and apoptosis in multiple myeloma, confirming our findings. In this publication, Tianhua et al claim that LINC00152 acts as a sponge, hence a negative regulator of miR497 [17].…”

Section: Positive Regulatory Feedback Between Stat3 and Stair18mentioning

confidence: 99%

Master and servant: LINC00152 – a STAT3-induced long noncoding RNA regulates STAT3 in a positive feedback in human multiple myeloma

et al. 2020

View full text Add to dashboard Cite

Background: The survival of INA-6 human multiple myeloma cells is strictly dependent upon the Interleukin-6activated transcription factor STAT3. Although transcriptional analyses have revealed many genes regulated by STAT3, to date no protein-coding STAT3 target gene is known to mediate survival in INA-6 cells. Therefore, the aim here was to identify and analyze non-protein-coding STAT3 target genes. In addition to the oncogenic microRNA-21, we previously described five long noncoding RNAs (lncRNAs) induced by STAT3, named STAiRs. Here, we focus on STAT3-induced RNA 18 (STAiR18), an mRNA-like, long ncRNA that is duplicated in the human lineage. One STAiR18 locus is annotated as the already well described LINC00152/CYTOR, however, the other harbors the MIR4435-2HG gene and is, up to now, barely described.Methods: CAPTURE-RNA-sequencing was used to analyze STAiR18 transcript architecture. To identify the STAiR18 and STAT3 phenotype, siRNA-based knockdowns were performed and microarrays were applied to identify their target genes. RNA-binding partners of STAiR18 were determined by Chromatin-Isolation-by-RNA-Purification (ChIRP) and subsequent sequencing. STAT3 expression in dependence of STAiR18 was investigated by immunoblots, chromatin-and RNA-immunoprecipitations. Results: As identified by CAPTURE-RNA sequencing, a complex splice pattern originates from both STAiR18 loci, generating different transcripts. Knockdown of the most abundant STAiR18 isoforms dramatically decreased INA-6 cell vitality, suggesting a functional role in myeloma cells. Additionally, STAiR18 and STAT3 knockdowns yielded overlapping changes of transcription patterns in INA-6 cells, suggesting a close functional interplay between the two factors. Moreover, Chromatin isolation by RNA purification (ChIRP), followed by genome-wide RNA sequencing showed that STAiR18 associates specifically with the STAT3 primary transcript. Furthermore, the knockdown of STAiR18 reduced STAT3 levels on both the RNA and protein levels, suggesting a positive feedback between both molecules. Furthermore, STAiR18 knockdown changes the histone methylation status of the STAT3 locus, which explains the positive feedback and indicates that STAiR18 is an epigenetic modulator.

show abstract

Long intergenic non‑protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA‑497

Cited by 10 publications

References 29 publications

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

Long noncoding RNA TUG1 promotes proliferation and inhibits apoptosis in multiple myeloma by inhibiting miR-29b-3p

Regulation of microRNA‑497 expression in human cancer (Review)

Master and servant: LINC00152 – a STAT3-induced long noncoding RNA regulates STAT3 in a positive feedback in human multiple myeloma

Contact Info

Product

Resources

About