Long noncoding RNAs: regulation, function and cancer

Rafiee, Aras; Riazi-Rad, Farhad; Havaskary, Mohammad; Nuri, Fatemeh

doi:10.1080/02648725.2018.1471566

Cited by 109 publications

(83 citation statements)

References 184 publications

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“…Mounting evidence has demonstrated that epigenetic regulation of lncRNAs plays important roles in human cancer progression, and may hold the key to developing novel molecular target for cancer treatment. [10][11][12] In the present study, we presented new data, showing lncRNA NORAD is upregulated in human EOC and inhibiting NORAD could yield tumor-suppressing functions in EOC cells through endogenously competition against hsa-miR-155-5p.…”

Section: Discussionmentioning

confidence: 70%

Retracted: Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR‐155‐5p

Tong

Zhang

et al. 2019

Cancer Medicine

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Purpose In the present study, we evaluated the expression and function of human long noncoding RNA (lncRNA) activated by DNA damage (NORAD) in human epithelial ovarian cancer (EOC). Methods NORAD expression was evaluated by qRT‐PCR in EOC cell lines and in situ EOC clinical samples. Lentivirus‐mediated NORAD downregulation was conducted in OVCAR‐3 and ES‐2 cells, and its effect on cancer cell proliferation, bufalin chemoresistance, cell‐cycle transition in vitro, and xenotransplantation in vivo were examined, respectively. The likelihood of an lncRNA‐microRNA (miRNA) signaling pathway was examined by probing the possible downstream competing target of NORAD, hsa‐miR‐155‐5p. Moreover, hsa‐miR‐155‐5p was knocked down in NORAD‐downregulated EOC cells to functionally evaluate the correlation between NORAD and hsa‐miR‐155‐5p in EOC. Results We found that NORAD was substantially upregulated in both EOC cell lines and human tumors. In OVCAR‐3 and ES‐2 cells, lentivirus‐mediated NORAD downregulation had significant anticancer effects, as it suppressed cell proliferation, decreased bufalin chemoresistance, arrested cell‐cycle transition, and inhibited xenograft growth. Also, hsa‐miR‐155‐5p was confirmed to be the competing target of NORAD in EOC, and its knockdown in OVCAR‐3 and ES‐2 cells reversed the NORAD downregulation‐induced anticancer functions. Conclusions NORAD is upregulated in EOC. Inhibition of NORAD, possibly through endogenously competing against hsa‐miR‐155‐5p, can be a new tumor‐suppressing strategy in EOC.

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Section: Discussionmentioning

confidence: 70%

Retracted: Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR‐155‐5p

Tong

Zhang

et al. 2019

Cancer Medicine

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“…On the other hand, miRNA, a class of short noncoding RNAs, have been shown to regulate translation of mRNAs by capturing them for degradation by RNA‐induced silencing complex or by sequestering them into GW/P‐bodies, stress granules, or other structures for later translation. Competing endogenous RNA, also known as ceRNAs (Rafiee et al, ), could bind to miRNAs and reduce its availability for binding to its target mRNA. In our study, we showed that lncRNA MALAT1 could sponge miR‐558, reducing its binding availability to ULK1 mRNA, in turn upregulating the expression levels of ULK1 mRNA.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, miRNA, a class of short noncoding RNAs, have been shown to regulate translation of mRNAs by capturing them for degradation by RNA-induced silencing complex or by sequestering them into GW/P-bodies, stress granules, or other structures for later translation. Competing endogenous RNA, also known as ceRNAs (Rafiee et al, 2018), could bind to miRNAs and F I G U R E 6 The effects of lncRNA MALAT1 on cardiomyocytes injuries in vivo. (a) WT-and MALAT1-knockout (MALAT1 −/− ) mice were treated with PBS or ISO as described in Section 2, and after they were killed, the expression levels of MALAT1 and miR-558 in myocardial tissues were determined by qRT-PCR.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1 protects cardiomyocytes from isoproterenol‐induced apoptosis through sponging miR‐558 to enhance ULK1‐mediated protective autophagy

Guo

Yan

et al. 2018

Journal Cellular Physiology

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Investigating the molecular mechanisms of myocardial infarction (MI) and subsequent heart failure have gained considerable attention worldwide. Long noncoding RNA (lncRNA) metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been previously demonstrated to regulate the proliferation and metastasis of several tumors. However, little is known about the effects of MALAT1 in MI and in regulating the cell date after MI. In our study, first, it was shown that the expression levels of MALAT1 were increased in the MI samples compared with normal tissues using quantitative reverse‐transcription polymerase chain reaction. Then, MALAT1 knockdown could significantly decrease the cell viability and increase the apoptotic rates in isoproterenol (ISO)‐treated H9C2 cells. In addition, we screened the possible target and found that miR‐558 is its direct target using dual luciferase reporter assay, indicating that MALAT1 functioned as decoys sponging miR‐558. Transfection of miR‐558 mimic decreased the cell viability and enhanced the apoptosis. Furthermore, we revealed that miR‐558 could downregulate ULK1 expression and suppressed ISO‐induced protective autophagy. Activation of MALAT1/miR‐558/ULK1 pathway protected H9C2 cells from ISO‐induced mitochondria‐dependent apoptosis. Finally, we used MALAT1‐knockout mice to further demonstrated that MALAT1 protected cardiomyocytes from apoptosis and partially improved the cardiac functions upon ISO treatment. In conclusion, we elucidated that lncRNA MALAT1 protected cardiomyocytes from ISO‐induced apoptosis by sponging miR‐558 thus promoting ULK1‐dependent autophagy. Targeting lncRNA MALAT1 might become a potential strategy in protecting cardiomyocytes during MI.

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“…The lncRNA field is in its infancy yet from what we do know we find that lncRNAs play critical roles in a wide variety of biological processes and diseases from cell differentiation, tissue organ development, flowering in plants, to cancer metastasis to name just a few [26][27][28][29][30]. We believe that lncRNAs play regulatory roles in many biological processes and diseases.…”

Section: The Biological Questionmentioning

confidence: 99%