LncRNA-mediated regulation of cell signaling in cancer

Peng, Wan-Xin; Koirala, Pratirodh; Mo, Yin‐Yuan

doi:10.1038/onc.2017.184

Cited by 1,363 publications

(1,071 citation statements)

References 87 publications

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“…The development and advancement of next-generation sequencing (NGS) technologies to various cancers has revealed thousands of ncRNAs has been revealed whose aberrant expression is associated with different cancer types [29][30][31]. An increasing number of studies indicate that diverse ncRNAs play a critical role in malignant transformation [32,33].…”

Section: Discussionmentioning

confidence: 99%

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

Qiu

Qiu³

et al. 2018

Cell Physiol Biochem

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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.

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Section: Discussionmentioning

confidence: 99%

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

Qiu

Qiu³

et al. 2018

Cell Physiol Biochem

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“…By total cellular RNA mass, lncRNA constitutes only 0.03-0.2% while mRNA constitute 3-7% (Dykes and Emanueli 2017). LncRNAs are classified based on their genomic organization: 1) intergenic lncRNAs (lincRNAs) are transcribed between two protein-coding genes; 2) intronic lncRNAs are transcribed from introns of protein-coding genes; 3) overlapping lncRNAs, as the name implies, constitute transcripts that overlap known protein-coding genes; and 4) antisense (as) lncRNAs are transcribed in a direction opposite that of the protein-coding gene (Peng, et al 2017b) ( Figure 2). Pseudogenes that arise from DNA duplication of coding genes followed by inactivating mutations that render the pseudogene non-coding are transcribed as lncRNAs and sequester some of the miRNAs that interact with conserved miRNA response elements (MREs) in the functional gene (Dykes and Emanueli 2017).…”

Section: Lncrnas: Classification and Functional Activitiesmentioning

confidence: 99%

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

Klinge

2018

Endocrine-Related Cancer

100

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Abstract:The human genome is 'pervasively transcribed' leading to a complex array of noncoding RNAs (ncRNAs) that far outnumber coding mRNAs. ncRNAs have regulatory roles in transcription and post-transcriptional processes as well numerous cellular functions that remain to be fully described. Best characterized of the 'expanding universe' of ncRNAs are the ~ 22 nucleotide microRNAs (miRNAs) that base-pair to target mRNA's 3' untranslated region within the RNA-induced silencing complex (RISC) and block translation and may stimulate mRNA transcript degradation. Long non-coding RNAs (lncRNAs) are classified as >200 nucleotides in length, but range up to several kb and are heterogeneous in genomic origin and function.LncRNAs fold into structures that interact with DNA, RNA, and proteins to regulate chromatin dynamics, protein complex assembly, transcription, telomere biology, and splicing. Some lncRNAs act as sponges for miRNAs and decoys for proteins. Nuclear-encoded lncRNAs can be taken up by mitochondria and lncRNAs are transcribed from mtDNA. Both miRNAs and lncRNAs are dysregulated in endocrine cancers. This review provides an overview on the current understanding of the regulation and function of selected lncRNAs and miRNAs, and their interaction, in endocrine-related cancers: breast, prostate, endometrial, and thyroid.

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“…A large proportion of lncRNAs transcribed in the opposite direction to the nearby genes may regulate their transcription for developmental regulation in pluripotent cells (Luo et al, ). LncRNAs play key roles in the oncogenesis and tumor progression either as oncogenes or tumor suppressors (Peng, Koirala, & Mo, ; C. C. Sun et al, ). Dysfunctions of lncRNAs occurred in various tumors and cell lines (Bhan, Soleimani, & Mandal, ; Kitagawa, Kotake, & Ohhata, ).…”

Section: Introductionmentioning

confidence: 99%

KCNQ1OT1 facilitates progression of non‐small‐cell lung carcinoma via modulating miRNA‐27b‐3p/HSP90AA1 axis

Dong

Yang²,

Qiu

et al. 2018

Journal Cellular Physiology

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Long noncoding RNA KCNQ1OT1 participates in the regulation of imprinted genes within the kcnq1 domain. But its roles in carcinogenesis and metastasis remain largely elusive. Herein, we evaluated its potential in non‐small‐cell lung cancer (NSCLC) progression. We demonstrated that the KCNQ1OT1 level was upregulated in NSCLC tissues and cell lines. High KCNQ1OT1 level correlated with poor overall and progression‐free survival in NSCLC patients. KCNQ1OT1 facilitated proliferation, migration, and invasion in H460 cells. Furthermore, knockdown of KCNQ1OT1 reduced the expression of HSP90AA1. KCNQ1OT1 presented a positive correlation with HSP90AA1 which predicted the tumor progression in NSCLC from The Cancer Genome Atlas database. Intriguingly, KCNQ1OT1 modulated HSP90AA1 expression by sponging miR‐27b‐3p. MiR‐27b‐3p counteracted the effect of KCNQ1OT1 on HSP90AA1 expression, H460 cell migration, and invasion. These data revealed a role for KCNQ1OT1 as an oncogene through miR‐27b‐3p/HSP90AA1 axis during NSCLC progression.

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LncRNA-mediated regulation of cell signaling in cancer

Cited by 1,363 publications

References 87 publications

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

KCNQ1OT1 facilitates progression of non‐small‐cell lung carcinoma via modulating miRNA‐27b‐3p/HSP90AA1 axis

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