Long non-coding RNAs: Functional regulatory players in breast cancer

Youness, R.A.; Gad, Mohamed Z.

doi:10.1016/j.ncrna.2019.01.003

Cited by 90 publications

(71 citation statements)

References 125 publications

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“…LncRNAs, a new kind of non-coding RNA, are longer than 200 nucleotides in length with no or limited protein-coding potential [6]. LncRNAs have been proved to play critical function in tumorigenesis through transcriptional levels to post-transcriptional levels [7,8]. lncRNAs are able to regulate the proliferation, apoptosis, migration and invasion of human cancer cells [9,10].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Hua

Deng

et al. 2020

J Exp Clin Cancer Res

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Background: Human ovarian cancer specific transcript 2 (HOST2) is a long non-coding RNA (lncRNA) reported to be specifically high expressed in human ovarian cancer. However, the mechanism that how HOST2 regulates triple negative breast cancer (TNBC) need to be explored. Methods: In this study, expression of HOST2 was determined in 40 TNBC patients and matched non-cancerous tissues by qRT-PCR and in situ hybridization (ISH) assay. The biological functions of HOST2 was measured by losing features. The effect of HOST2 on viability, proliferation and migration was evaluated by MTT, colony formation assay, EDU analysis, transwell invasion assay and nude mouse xenograft model. Fluorescence in situ hybridization (FISH), Luciferase report assay, RNA immunoprecipitation (RIP) assay and Western blot were fulfilled to measure molecular mechanisms. Results: The results showed that HOST2 was up-regulated in BC tissues and cell lines. Clinical outcome analysis demonstrated that high expression of HOST2 was associated with poor prognosis of TNBC patients. Functional experiments illustrated that knockdown of HOST2 significantly suppressed TNBC cell proliferation and migration. Western blot assays, qRT-PCR assays, RIP assays and luciferase reporter assays revealed that HOST2 regulated STAT3 via crosstalk with let-7b. Depression of HOST2 suppressed STAT3-mediated proliferation and migration in TNBC cells. HOST2 could function as a decoy of let-7b to depress expression of STAT3. Conclusions: HOST2 could function as a oncogene and promoted STAT3-mediated proliferation and migration through acting as a competing endogenous RNA, which might act as a potential biomarker for TNBC patients.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Hua

Deng

et al. 2020

J Exp Clin Cancer Res

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“…[9][10][11][12] Their dysfunction and specific role in various diseases, especially cancer, have attracted more and more attention recently. [13][14][15] LncRNAs genomic mutants or alteration have been widely clarified to induce oncogenic effect in multiple cancer types, such as breast cancer, 16 colorectal cancer, 17 ovarian cancer, 18 gastric cancer, 19 lung cancer, 20 as well as AML. 21,22 Several lncRNAs, including lnc_071255/Pvt1, lnc_104449, or lnc_177417, are found essential for AML maintenance and normal differentiation.…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

Dong

Guan

2020

Cell Biochemistry & Function

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Long non‐coding RNA (lncRNA) LINC00899 is one kind cytoplasmic lncRNA, however, there is rarely little information about its function in physiological process. Here, we demonstrated that lncRNA LINC00899 was upregulated in acute myeloid leukaemia (AML) cells and was quite correlated with poor prognosis of AML patients. High expression of LINC00899 in AML cells could promote cell proliferation and inhibit cell apoptosis, and facilitate the progression of AML consequently both in vitro and in vivo. Besides, LINC00899 acted as a molecular sponge of miR‐744‐3p. Furthermore, we characterized YY1 as the direct target of miR‐744‐3p, and LINC00899/miR‐744‐3p interaction modulated YY1 expression in AML cells. Finally, we verified LINC00899 modulated AML cell proliferation and apoptosis via regulating YY1. Our study revealed novel mechanism about how did lncRNA LINC00899 execute function in AML and thus provided potential therapeutic interventions for AML.Significance of the study LncRNA LINC00899 is upregulated in AML cells and is correlated with poor prognosis of AML patients. LncRNA LINC00899 mediates cell proliferation and apoptosis of acute myeloid leukaemia cells. Knockdown of LINC00899 inhibited the growth of xenograft glioma tumour in vivo. LINC00899 acts as a molecular sponge of miR‐744‐3p. YY1 is the downstream target of LINC00899/miR‐744‐3p signalling.

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“…A large number of evidences suggest that LncRNAs are important to the regulation of cell differentiation, proliferation, and apoptosis (Tay et al 2014). It is also known that aberrant expression of LncRNAs have crucial roles in the initiation and development of various human cancers, including breast cancer (Youness and Gad 2019). In this study, we found that MT1JP expression was down-regulated in breast cancer cell lines.…”

Section: Discussionmentioning

confidence: 53%

Long non-coding RNA MT1JP exerts anti-cancer effects in breast cancer cells by regulating miR-92-3p

H¹,

Li²

2020

gpb

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MT1JP is a LncRNA that is reportedly involved in gastric cancer development, but a biological role and mechanism for MT1JP in breast cancer is unknown. Quantitative RT-PCR was performed to detect the level of MT1JP and miR-92a-3p, and Western blotting assays ware performed to measure the expression of CDK2, cyclinE1, P21, CD151, CD147, MMP2 and MMP9 in breast cells. Subsequently, cell viability was analyzed with CCK-8 assay. Cell migration and invasion were analyzed with Transwell and Scratch Test, respectively. The results demonstrated that MT1JP was significantly down-regulated in breast cells. Additionally, we found that overexpression of MT1JP in breast cancer cells significantly inhibited cell proliferation, migration and invasion, and regulate the expression of CDK2, cyclinE1 and P21. We then investigated a possible mechanism for these results, MT1JP significantly inhibited CD151, CD147, MMP2 and MMP9 protein expression in breast cancer cells. Moreover, we found that MT1JP binds to and negatively regulates miR-92-3p, which is known to be an oncogene in some human cancers. Our data indicate that MT1JP functions as an anti-tumor LncRNA and downregulates miR-92-3p, CD151 and CD147, and may serve as a novel diagnostic and therapeutic marker in breast cancer.

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Long non-coding RNAs: Functional regulatory players in breast cancer

Cited by 90 publications

References 125 publications

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

LncRNA LINC00899 promotes progression of acute myeloid leukaemia by modulating miR‐744‐3p/YY1 signalling

Long non-coding RNA MT1JP exerts anti-cancer effects in breast cancer cells by regulating miR-92-3p

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