Crosstalk between Long Noncoding RNAs and MicroRNAs in Health and Disease

Bayoumi, Ahmed S.; Sayed, Amer; Broskova, Zuzana; Teoh, Jian Peng; Wilson, James M.; Su, Huabo; Tang, Yaoliang; Kim, Il-man

doi:10.3390/ijms17030356

Cited by 208 publications

(152 citation statements)

References 87 publications

Supporting

Mentioning

148

Contrasting

Order By: Relevance

“…It has been demonstrated that miRNAs can be downregulatedted through complementing with long noncoding RNAs (lncRNAs) (12). In this study, we found a negative relationship between long noncoding RNA TUG1 (lncRNA-TUG1) and miR-381 in GC tissues (P<0.01, Fig.…”

Section: Mir-381 Was Negatively Regulated By Long Noncoding Rna Tug1mentioning

confidence: 60%

See 1 more Smart Citation

MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4

Zhang¹,

Huang²,

Long³

2017

Oncology Letters

View full text Add to dashboard Cite

Abstract. Aberrant expression of microRNAs (miRs) serves essential roles in the generation and progression of various types of human cancer. In the present study, the expression and biological functions of miR-381 in human gastric carcinoma (GC) were focused upon. The results of reverse transcription-quantitative polymerase chain reaction analysis revealed that the expression of miR-381 was significantly downregulated in GC tissue samples. Furthermore, low expression of miR-381 was identified to be associated with lymphatic metastasis and advanced tumor-node-metastasis stage (III+IV). Upregulation of miR-381 inhibited the migration and invasion of GC SGC-7901 cells through SRY-Box 4 (SOX4)-mediated epithelial-mesenchymal transition. Finally, long non-coding (lnc) RNA-taurine upregulatedted 1 (non-protein coding) (TUG1) was confirmed as a negatively regulator of miR-381 expression in SGC-7901 cells. Taken together, the results of the current study indicate that the downregulation of miR-381 by lncRNA-TUG1 promoted the metastasis of GC cells by inhibiting SOX4. Thus, targeting miR-381 may be a novel therapeutic option for the treatment of patients with GC.

show abstract

Section: Mir-381 Was Negatively Regulated By Long Noncoding Rna Tug1mentioning

confidence: 60%

“…However, the expression and functions of miR-381 in gastric carcinoma are still unclear. Recently, long noncoding RNAs (lncRNAs) were found to act as a sponge of microRNAs and regulate the expression and function of microRNAs (12), but there is still no study to investigate whether miR-381 can be regulated by lncRNAs.…”

Section: Introductionmentioning

confidence: 99%

MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4

Zhang¹,

Huang²,

Long³

2017

Oncology Letters

View full text Add to dashboard Cite

show abstract

“…These RNAs may work in gene regulatory networks as signals, decoys, guides or scaffold [46][47][48], and coordinate histone modifications by binding to various histone modification enzymes such as PRC2, which is a methyltransferase for H3K27me3 and is involved in the repression of gene transcription [49][50][51]. EZH2 is a catalytic subunit of PRC2 [52].…”

Section: Discussionmentioning

confidence: 99%

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

Qiu

Qiu³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: SNHG6 (Small Nucleolar RNA Host Gene 6) is a novel non-coding RNA (ncRNA) and its cellular function is largely unknown. Methods: Cell Counting Kit-8 (CCK-8) cell growth assay, colony formation and flow cytometry were used to determine colorectal cancer cell proliferation, cell cycle progression and apoptosis in vitro. The xenograft tumor formation assay in nude mice was established to evaluate tumor growth in vivo. RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter. Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. Survival analysis suggested that higher expression of SNHG6 predicted poor prognosis in patients with colorectal cancer. Functional studies indicated that SNHG6 could promote cell proliferation via a direct suppression of p21 expression in colorectal cancer cells. Moreover, SNHG6 repressed p21 transcription through recruiting EZH2 to the p21 promoter in colorectal cancer cells. Conclusion: Taken together, our study demonstrates that SNHG6 promotes tumor growth via repression of p21 in colorectal cancer, which may provide a promising target for novel anticancer therapeutics.

show abstract

“…miRNAs have been considered as oncogenes or tumor suppressors by regulating cell proliferation and differentiation [20]. The crosstalk between lncRNAs and miRNAs has been reported to control cancer progression [21]. miR-203a has been found to be a crucial regulator involved in various cancers, such as gastric cancer [22], nasopharyngeal carcinoma [23], breast cancer [24], lung cancer [25], live cancer [26], and CRC [27].…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/ß-Catenin Signaling Pathway

Xiao

Chen

et al. 2018

Cell Physiol Biochem

132

View full text Add to dashboard Cite

Background/Aims: HOX transcript antisense RNA (HOTAIR) plays a vital role in carcinogenesis. However, its functional and regulatory roles remain unclear. In this study, we aimed to investigate its biological function and clinical significance in human colorectal cancer (CRC). Methods: We examined the expression levels of lncRNA HOTAIR and miR-203a-3p in CRC tissues and CRC cell lines by qRT-PCR. Gain and loss-of-function assays were performed to examine the effects of HOTAIR and miR-203a-3p on the proliferation and chemoresistance of CRC cells. The possible mechanisms of HOTAIR were also explored by fluorescence reporter assay and Western blot. Results: The expressions of HOTAIR were upregulated in CRC tissue tissues compared to adjacent control tissues. We also found HOTAIR was downregulated by miR-203a-3p in CRC cell lines. Both HOTAIR knockdown and miR-203a-3p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that β-catenin and GRG5 were inhibitory targets of miR-203a-3p, and that Wnt/β-catenin signaling was inhibited by both HOTAIR knockdown and miR-203a-3p overexpression. Significantly, we found that increased expression of miR-203a-3p is essential for cell proliferation repression, chemoresistance reduction, and Wnt/β-catenin signaling inhibition induced by HOTAIR knockdown. Conclusions: Our study demonstrated that the lncRNA HOTAIR could regulate the progression and chemoresistance of CRC via modulating the expression levels of miR-203a-3p and the activity of Wnt/β-catenin signaling pathway.

show abstract

Crosstalk between Long Noncoding RNAs and MicroRNAs in Health and Disease

Cited by 208 publications

References 87 publications

MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4

MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/ß-Catenin Signaling Pathway

Contact Info

Product

Resources

About