Long non‑coding RNA NEAT1 modifies cell proliferation, colony formation, apoptosis, migration and invasion via the miR‑4500/BZW1 axis in ovarian cancer

Xu, Huibin; Sun, Xiaowei; Huang, Ying; Qin, Si; Li, Maokun

doi:10.3892/mmr.2020.11408

Cited by 19 publications

(14 citation statements)

References 39 publications

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“…In addition to the promotion of OC cell proliferation, migration, and invasion, NEAT1 was shown to inhibit OC cell apoptosis by upregulating the expression of basic leucine zipper and W2 domain-containing protein 1 (BZW1) via interaction with miR-4500 [84]. NEAT1 also enhanced EMT of OC cells by upregulating the expression of tight junction protein 3 (TJP3) via interaction with miR-1321 [85].…”

Section: Ovarian Cancermentioning

confidence: 99%

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Yao

et al. 2021

Int. J. Biol. Sci.

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The nuclear paraspeckle assembly transcript 1 (NEAT1) is a long non-coding RNA (lncRNA) that is upregulated in a variety of human cancer types. Increasing evidence has shown that the elevation of NEAT1 in cancer cells promotes cell growth, migration, and invasion and inhibits cell apoptosis. It is also known that lncRNAs act as a competing endogenous RNA (ceRNA) by sponging microRNAs (miRNAs) to alter the expression levels of their target genes in the development of cancers. Therefore, it is important to understand the molecular mechanisms underlying this observation. In this review, specific emphasis was placed on NEAT1's role in tumor development. We also summarize and discuss the feedback roles of NEAT1/miRNA/target network in the progression of various cancers. As our understanding of the role of NEAT1 during tumorigenesis improves, its therapeutic potential as a biomarker and/or target for cancer also becomes clearer.

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Section: Ovarian Cancermentioning

confidence: 99%

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Yao

et al. 2021

Int. J. Biol. Sci.

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“…Another study has also reported the implication of NEAT1 in the tumorigenesis and development of ovarian cancer [ 10 ]. Additionally, NEAT1 knockdown has been reported to suppress ovarian cancer cell proliferation, colony formation, migration, and invasion while stimulating cell apoptosis [ 11 ]. Furthermore, NEAT1 can target microRNA let-7 g-5p (miR let-7 g-5p) and negatively regulate its expression in glioblastoma [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA NEAT1 facilitates the growth, migration, and invasion of ovarian cancer cells via the let-7 g/MEST/ATGL axis

Yin

Wang

2021

Cancer Cell Int

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Background/Aim Growing evidence indicates a significant role of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) in ovarian cancer, a frequently occurring malignant tumor in women; however, the possible effects of an interplay of NEAT1 with microRNA (miRNA or miR) let-7 g in ovarian cancer are not known. The current study aimed to investigate the role of the NEAT1/let-7 g axis in the growth, migration, and invasion of ovarian cancer cells and explore underlying mechanisms. Methods NEAT1 expression levels were examined in clinical tissue samples and cell lines. The relationships between NEAT1, let-7 g, and MEST were then analyzed. Gain- or loss-of-function approaches were used to manipulate NEAT1 and let-7 g. The effects of NEAT1 on cell proliferation, migration, invasion, and apoptosis were evaluated. Mouse xenograft models of ovarian cancer cells were established to verify the function of NEAT1 in vivo. Results NEAT1 expression was elevated while let-7 g was decreased in ovarian cancer clinical tissue samples and cell lines. A negative correlation existed between NEAT1 and let-7 g, whereby NEAT1 competitively bound to let-7 g and consequently down-regulate let-7 g expression. By this mechanism, the growth, migration, and invasion of ovarian cancer cells were stimulated. In addition, let-7 g targeted mesoderm specific transcript (MEST) and inhibited its expression, leading to promotion of adipose triglyceride lipase (ATGL) expression and inhibition of ovarian cancer cell growth, migration, and invasion. However, the effect of let-7 g was abolished by overexpression of MEST. Furthermore, silencing of NEAT1 decreased the xenograft tumor growth by decreasing MEST while up-regulating let-7 g and ATGL. Conclusions Cumulatively, the findings demonstrated that NEAT1 could promote malignant phenotypes of ovarian cancer cells by regulating the let-7 g/MEST/ATGL signaling axis. Therefore, NEAT1 can be regarded as an important molecular target and biomarker for ovarian cancer.

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“…In OC, NEAT1 promotes cancer cell proliferation, invasion, migration, EMT, and angiogenesis by regulating the expression of a wide variety of miRNAs and associated pathways. For example, upregulation of the FGF9 pathway by sponging miR-365 [ 139 ], regulation of TJP3 expression by interacting with and sponging miR-1321 [ 140 ], alteration of cancer proliferation, apoptosis and colony formation by regulation of miR-4500/BZW1 axis [ 141 ], and by sponging many other miRNAs [ 142 ]. Moreover, in a study involving 18 cisplatin-sensitive and 19 cisplatin-resistant OC patients, overexpressed NEAT1 was reported to induce cisplatin resistance ( p = 0.031) in OC cells via the regulation of miR-770-5p and PARP1 [ 143 ].…”

Section: Lncrnas In Female-oriented Cancersmentioning

confidence: 99%

The Role of Long Non-Coding RNAs (lncRNAs) in Female Oriented Cancers

Naz

Tariq

Ali

et al. 2021

Cancers

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Recent advances in molecular biology have discovered the mysterious role of long non-coding RNAs (lncRNAs) as potential biomarkers for cancer diagnosis and targets for advanced cancer therapy. Studies have shown that lncRNAs take part in the incidence and development of cancers in humans. However, previously they were considered as mere RNA noise or transcription byproducts lacking any biological function. In this article, we present a summary of the progress on ascertaining the biological functions of five lncRNAs (HOTAIR, NEAT1, H19, MALAT1, and MEG3) in female-oriented cancers, including breast and gynecological cancers, with the perspective of carcinogenesis, cancer proliferation, and metastasis. We provide the current state of knowledge from the past five years of the literature to discuss the clinical importance of such lncRNAs as therapeutic targets or early diagnostic biomarkers. We reviewed the consequences, either oncogenic or tumor-suppressing features, of their aberrant expression in female-oriented cancers. We tried to explain the established mechanism by which they regulate cancer proliferation and metastasis by competing with miRNAs and other mechanisms involved via regulating genes and signaling pathways. In addition, we revealed the association between stated lncRNAs and chemo-resistance or radio-resistance and their potential clinical applications and future perspectives.

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Long non‑coding RNA NEAT1 modifies cell proliferation, colony formation, apoptosis, migration and invasion via the miR‑4500/BZW1 axis in ovarian cancer

Cited by 19 publications

References 39 publications

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

NEAT1 as a competing endogenous RNA in tumorigenesis of various cancers: Role, mechanism and therapeutic potential

Long non-coding RNA NEAT1 facilitates the growth, migration, and invasion of ovarian cancer cells via the let-7 g/MEST/ATGL axis

The Role of Long Non-Coding RNAs (lncRNAs) in Female Oriented Cancers

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