Long non-coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR-377 in non-small cell lung cancer

Zhang, Junsheng; Li, Yongli; Dong, Mei; Wu, Dongyuan

doi:10.3892/ol.2017.6769

Cited by 60 publications

(42 citation statements)

References 35 publications

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“…10 A member of the lncRNA, nuclear enriched abundant transcript 1 (NEAT1) is reported as an oncogene in various malignant tumors, including hepatocellular carcinoma, non-small cell lung cancer, nasopharyngeal carcinoma, breast cancer and OC. [11][12][13][14][15][16] report that NEAT1 contributed Yangcheng Liu and Yong Wang contributed equally to this work. to paclitaxel (PTX) resistance of OC cells through upregulating ZEB1 expression by sponging of .…”

Section: Introductionmentioning

confidence: 98%

Long non‐coding RNA NEAT1 promoted ovarian cancer cells’ metastasis through regulation of miR‐382‐3p/ROCK1 axial

et al. 2018

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Long non‐coding RNA (lncRNA) are extensively involved in various malignant tumors, including ovarian cancer (OC). In the present study, we focused on the expression and function of nuclear enriched abundant transcript 1 (NEAT1) in OC cells’ metastasis. We demonstrated that NEAT1 was upregulated in OC tissue specimens and cell lines. In addition, we revealed that depression of NEAT1 inhibited OC cells’ metastasis and the expression of Rho associated coiled‐coil containing protein kinase 1 (ROCK1), which is a metastasis‐related gene. Using online predictive software and a series of luciferase assays, we demonstrated that both NEAT1 and ROCK1 were the targets of microRNA‐382‐3p (miR‐382‐3p) and share similar microRNA responding elements (MRE). Furthermore, we illustrated that NEAT1 and miR‐382‐3p inhibited each other in a reciprocal manner. Finally, through antisense experiments we demonstrated that NEAT1 promoted ROCK1‐mediated metastasis by functioning as a ceRNA of miR‐382‐3p. In summary, the findings of this study revealed that NEAT1 promoted OC cells’ metastasis through regulating the miR‐382‐3p/ROCK1 axial. The present study might provide a new target for treating OC.

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Section: Introductionmentioning

confidence: 98%

Long non‐coding RNA NEAT1 promoted ovarian cancer cells’ metastasis through regulation of miR‐382‐3p/ROCK1 axial

et al. 2018

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“…E2F3 (Fig. 3A) was predicted as a primary target of miR-433 and selected for investigation, to further verify its previously reported contribution to NSCLC formation and progression (26)(27)(28)(29)(30). To confirm this hypothesis, luciferase reporter assays were performed using A549 and H460 cells cotransfected with miR-433 mimics or miR-NC and pMIR-Wt-E2F3-3'-UTR or pMIR-Mut-E2F3-3'-UTR.…”

Section: E2f3 Is a Direct Target Of Mir-433 In Nsclcmentioning

confidence: 79%

MicroRNA‑433 reduces cell proliferation and invasion in non‑small cell lung cancer via directly targeting E2F transcription factor 3

Liu

Zhang

et al. 2018

Mol Med Report

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MicroRNAs (miRNA/miRs) have been associated with the initiation and progression of non‑small‑cell lung cancer (NSCLC). Hence, a comprehensive understanding of the association between dysregulated miRNAs and NSCLC may contribute to the identification of novel therapeutic methods for patients with NSCLC. MiRNA‑433 (miR‑433) has been reported to be dysregulated in numerous types of human cancers; however, its expression pattern, biological roles and associated mechanisms in NSCLC require further investigation. The present study aimed to detect miR‑433 expression and determine its roles and underlying molecular mechanisms in NSCLC. In the present study, reverse transcription‑quantitative polymerase chain reaction revealed that miR‑433 was significantly downregulated in NSCLC tissues and cell lines. This decreased miR‑433 expression was strongly associated with the tumor node metastasis stage and lymph node metastasis of patients with NSCLC. Cell Counting kit‑8 and cell invasion assays revealed that the resumption of miR‑433 expression decreased the proliferation and invasion of NSCLC cells. Bioinformatics analysis predicted E2F transcription factor 3 (E2F3) as a potential target of miR‑433. Luciferase reporter assay, RT‑qPCR and western blot analysis further demonstrated that E2F3 was a direct target of miR‑433 in NSCLC. E2F3 downregulation induced by small interfering RNA exhibited inhibitory effects similar to those of miR‑433 overexpression in NSCLC cells, and the restored E2F3 expression counteracted the suppressive effects on NSCLC cells induced by miR‑433 overexpression. Therefore, miR‑433 may inhibit the progression of NSCLC, at least in part, by targeting E2F3. The present study indicated that miR‑433 may be investigated as an innovative candidate target for the therapy of patients with this fatal disease.

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“…For example, miR‐203a inhibits gastric cancer cell proliferation by targeting E2F3 24 . LncRNA NEAT1 modulates non–small cell lung cancer progression by sponging miR‐377 to regulate the E2F3 expression 25 . E2F3 has been reported to be linked with RB 14 .…”

Section: Discussionmentioning

confidence: 99%

Circular RNA (circ‐0075804) promotes the proliferation of retinoblastoma via combining heterogeneous nuclear ribonucleoprotein K (HNRNPK) to improve the stability of E2F transcription factor 3 E2F3

Zhao

Wang

Qin

et al. 2020

J of Cellular Biochemistry

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It is growingly recognized that messenger RNAs (mRNAs) are important regulators of various cancers. However, there are few reporters about the function of E2F3 in retinoblastoma (RB), which needs more exploration. In addition, the circRNA circ-0075804 was derived from the E2F3 host gene. The purpose of the study is to figure out the role and molecular regulation mechanism of E2F3 and circ-0075804 in RB. The role of E2F3 in RB was determined through E2F3 silencing and loss of expression was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR), Western blot, CCK-8, colony formation, and 5-ethynyl-2′-deoxyuridine assays. The interactions between E2F3 and circ-0075804 were validated through loss and gain function of circ-0075804. Besides, the role of circ-0075804 in RB was determined by several functional assays. And the binding ability between heterogeneous nuclear ribonucleoprotein K and circ-0075804 was verified by RNA pull-down, Western blot, and RT-qPCR assays. The expression of E2F3 was upregulated in RB cell lines. Furthermore, knockdown of E2F3 inhibited cell proliferation and induced cell apoptosis in RB. And circ-0075804 positively regulated the expression of E2F3. Moreover, circ-0075804 facilitated cell proliferation and suppressed cell apoptosis. Besides, HNRNPK could bind with circ-0075804 in RB. Finally, knockdown of E2F3 partly rescued the promoting role of circ-0075804 overexpression in RB. Overall, circ-0075804 promotes the proliferation of RB via combining HNRNPK to improve the stability of E2F3, which brings new light for treating RB. K E Y W O R D S circ-0075804, E2F3, HNRNPK, retinoblastoma

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Long non-coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR-377 in non-small cell lung cancer

Cited by 60 publications

References 35 publications

Long non‐coding RNA NEAT1 promoted ovarian cancer cells’ metastasis through regulation of miR‐382‐3p/ROCK1 axial

Long non‐coding RNA NEAT1 promoted ovarian cancer cells’ metastasis through regulation of miR‐382‐3p/ROCK1 axial

MicroRNA‑433 reduces cell proliferation and invasion in non‑small cell lung cancer via directly targeting E2F transcription factor 3

Circular RNA (circ‐0075804) promotes the proliferation of retinoblastoma via combining heterogeneous nuclear ribonucleoprotein K (HNRNPK) to improve the stability of E2F transcription factor 3 E2F3

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