Noncoding RNA:RNA Regulatory Networks in Cancer

Chan, Jia Jia; Tay, Yvonne

doi:10.3390/ijms19051310

Cited by 878 publications

(688 citation statements)

References 183 publications

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“…Antisense transcription is from the opposite strand of a protein‐coding gene or a sense strand‐derived RNA. Emerging studies show that antisense lncRNA (lncRNA‐AS) can function as positive or negative regulators of coding genes to further modulate cancer progression via miRNA decoys or competing endogenous RNA (ceRNA) and other mechanisms …”

Section: Introductionmentioning

confidence: 99%

LncRNA TPT1‐AS1 promotes tumorigenesis and metastasis in epithelial ovarian cancer by inducing TPT1 expression

Wei

Gao

et al. 2019

Cancer Science

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Increasing numbers of studies have confirmed that long noncoding RNA (lnc RNA ) play a critical role in epithelial ovarian cancer ( EOC ) progression. However, the potential function of the lnc RNA tumor protein translationally controlled 1 ( TPT 1) antisense RNA 1 ( TPT 1‐ AS 1) in EOC is unclear. In this study, we aimed to uncover the biological roles and regulatory mechanisms of TPT 1‐ AS 1 in EOC progression and metastasis. First, TPT 1‐ AS 1 expression was significantly higher in EOC metastatic tissue and cell lines than in their respective control counterparts. In addition, ectopic TPT 1‐ AS 1 expression was strongly associated with unfavorable EOC clinicopathological features, including FIGO stage, tumor size and tumor differentiation. TPT 1‐ AS 1 overexpression remarkably induced cell proliferation, migration and invasion, and significantly attenuated cell adhesion ability in vitro and facilitated nude mouse subcutaneous xenograft growth and intraperitoneal metastasis in vivo, while the downregulation of TPT 1‐ AS 1 expression produced the opposite effect in vitro. Mechanistically, TPT 1‐ AS 1 was proven to be primarily distributed in EOC cell nuclei and positively modulated TPT 1 promoter activity and transcription. Moreover, the oncogenic effects of TPT 1‐ AS 1 could be reversed by TPT 1 depletion, and the PI 3K/ AKT signaling pathway downstream of TPT 1 was also altered. These results suggested that TPT 1‐ AS 1 induced EOC tumor growth and metastasis through TPT 1 and downstream PI 3K/ AKT signaling and that TPT 1‐ AS 1 may be a promising therapeutic target for EOC .

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Section: Introductionmentioning

confidence: 99%

LncRNA TPT1‐AS1 promotes tumorigenesis and metastasis in epithelial ovarian cancer by inducing TPT1 expression

Wei

Gao

et al. 2019

Cancer Science

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“…Recent studies have illuminated that LncRNAs can function as a kind of ceRNA to interact with miRNAs and further regulate the expression of target mRNAs through sharing miRNA response elements (MREs) . Thus, LncRNA‐miRNA‐mRNA forms a novel regulatory network at post‐transcription level .…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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Long non‐coding RNA (LncRNA) MEG3 serves a regulatory role in the progression of several types of cancer, but the role of MEG3 in laryngeal cancer is still unknown. The aim of this study was to explore the regulatory role and mechanism of MEG3 in laryngeal cancer. MEG3 expression in 50 laryngeal cancer tissue samples was detected by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR). The effects of MEG3 overexpression on laryngeal cancer cells were investigated in vitro and in vivo. The mechanism of competitive endogenous RNA (ceRNA) was validated through luciferase reporter assay, RT‐qPCR and Western blotting. MEG3 was down‐regulated in laryngeal cancer tissues, and the low MEG3 expression was associated with advanced clinical stage. Additionally, MEG3 overexpression inhibited the proliferation and induced the apoptosis of laryngeal cancer cells in vitro and in vivo. Particularly, MEG3 bound to miR‐23a specifically and a reciprocal negative regulation existed between miR‐23a and MEG3. Moreover, MEG3 up‐regulated apoptotic protease activating factor‐1 (APAF‐1), a known miR‐23a's target, thereby leading to the activation of caspase‐9 and caspase‐3. Meanwhile, these activated effects were rescued by miR‐23a overexpression. In conclusion, the present study demonstrated that MEG3 functions as a novel tumour suppressive LncRNA in laryngeal cancer for the first time. Furthermore, MEG3 may act as a ceRNA to regulate APAF‐1 expression by competitive binding to miR‐23a, thereby regulating the progression of laryngeal cancer.

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“…[1][2][3] Dysfunction of several lncRNAs have been found to be associated with human ovarian cancer. [1][2][3] Dysfunction of several lncRNAs have been found to be associated with human ovarian cancer.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

Yan

Silva

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) have been reported to be abnormally expressed in several cancers and associated with the proliferation of cancer cells. The objective of this study was to investigate the role and the underlying mechanisms of DQ786243 in ovarian cancer. In the current study, DQ786243 was specifically upregulated in ovarian cancer tissues and cell lines. Knockdown of DQ786243 inhibited the ability of cell migration, invasion, proliferation, colony formation and wound healing, whereas promoted cell apoptosis and induced G0/G1 cell cycle arresting. By using online tools and mechanistic analysis, we demonstrated that DQ786243 could directly bind to microRNA-506 (miR-506) and downregulate its expression. Moreover, DQ786243 reversed the inhibitory effect of miR-506 on the growth of ovarian cancer cells, which might be involved in the derepression of cAMP responsive element binding protein 1 (CREB1) expression. Further investigation into the mechanisms showed that knockdown of DQ786243 inhibited the epithelial to mesenchymal transition (EMT) process in ovarian cancer cells. Finally, xenograft experiments further confirmed that knockdown of DQ786243 notably suppressed the proliferation and EMT process in vivo. Taken together, our study showed for the first time that DQ786243 interacted with miR-506 and promoted progression of ovarian cancer via targeting CREB1 in ovarian cancer. The results might help to probe the feasibility of lncRNA-directed therapy for this deadly disease.

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Noncoding RNA:RNA Regulatory Networks in Cancer

Cited by 878 publications

References 183 publications

LncRNA TPT1‐AS1 promotes tumorigenesis and metastasis in epithelial ovarian cancer by inducing TPT1 expression

LncRNA TPT1‐AS1 promotes tumorigenesis and metastasis in epithelial ovarian cancer by inducing TPT1 expression

LncRNA MEG3 inhibits cell proliferation and induces apoptosis in laryngeal cancer via miR‐23a/APAF‐1 axis

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

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