miR‐15a‐5p, miR‐15b‐5p, and miR‐16‐5p inhibit tumor progression by directly targeting MYCN in neuroblastoma

Chava, Srinivas; Reynolds, C. Patrick; Pathania, Anup Singh; Gorantla, Santhi; Poluektova, Larisa Y.; Coulter, Donald W.; Gupta, Subash C.; Pandey, Manoj K.; Challagundla, Kishore B.

doi:10.1002/1878-0261.12588

Cited by 106 publications

(80 citation statements)

References 70 publications

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“…3e, f). Ago2, an important component of RNA induced silencing complex (RISC), generally interacts with RNAs [31,32]. Then a RIP binding assay was conducted by using anti-Ago2 antibody in 293 T cell line, the results showed that the level of HOST2 and let-7b/miR-1266 was higher in anti-Ago2 group than that in anti-normal IgG group (Fig.…”

Section: Host2 Acted As a Sponge Of Let-7b And Mir-1266 In Tnbc Cellsmentioning

confidence: 98%

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: Host2 Acted As a Sponge Of Let-7b And Mir-1266 In Tnbc Cellsmentioning

confidence: 98%

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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“…For example, lncRNA CR749391 was reported to promote the progression of gastric cancer by sponging miR-181a ( 28 ); lncRNA HCG18 promotes the development of NPC by functioning as a ceRNA of miR-16 to upregulate G1/S-specific cyclin-D1 expression levels ( 29 ) and lncRNA AFAP1-AS1 was observed to function as a ceRNA of miR-423-5p to promote NPC metastasis by activating the Rho/Rac signaling pathway ( 30 ). Previous studies have also indicated that miR-16 is associated with cancer regulation, including cervical cancer, bladder cancer and neuroblastoma ( 31 – 33 ). Consistent with these findings, the present study also observed an interaction between KIF9-AS1 and miR-16 through a series of experiments.…”

Section: Discussionmentioning

confidence: 98%

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

You

Wang

2020

Oncol Lett

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Long non-coding RNAs (lncRNAs) have been reported to serve a crucial role in the progression of nasopharyngeal carcinoma (NPC); however, the underlying molecular mechanisms of lncRNA KIF9-AS1 in the tumorigenesis of NPC remains poorly understood. Reverse transcription-quantitative PCR was used to analyze the expression levels of KIF9-AS1 and microRNA (miR)-16, and Cell Counting Kit-8, wound healing and Transwell assays were used to determine the cell viability, invasion and migration, respectively, of NPC cells. In addition, a dual-luciferase reporter assay was used to analyze the direct interaction between KIF9-AS1 and miR-16. NPC stage was classified according to the seventh edition of the AJCC staging system. The results revealed that KIF9-AS1 expression levels were upregulated in NPC tissues and cell lines. In addition, miR-16 was demonstrated to directly interact with KIF9-AS1 and inhibit KIF9-AS1 expression levels, whereas the miR-16 inhibitor rescued the effects of the KIF9-AS1-knockdown in NPC cells. Furthermore, the expression levels of KIF9-AS1 were upregulated, while those of miR-16 were downregulated in NPC tissues. Notably, the expression levels of KIF9-AS1 were observed to be significantly more upregulated in advanced tumors (III–IV vs. I–II) and patients with high KIF9-AS1 expression levels exhibited a worse prognosis. In conclusion, the findings of the present study suggested that KIF9-AS1 may promote the progression of NPC by targeting miR-16, thus KIF9-AS1 may be a novel molecular target for NPC therapy.

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“…The inhibitory effects of mir-15b-5p have been revealed in neuroblastoma, and it can restrain tumor progression by directly targeting MYcn proto-oncogene, bHlH transcription factor (18). luo et al (42) demonstrated that mir-15b-5p reduced proliferation, but induced apoptosis and cytotoxic activities of Pc12 cells.…”

Section: Discussionmentioning

confidence: 99%

“…as a mature mirna, mir-15b-5p is spliced from the 5'-end of pre-mir-15b, which is a member of mir-16 family (15,16). Moreover, mir-15b-5p is upregulated in gastric cancer (15), liver cancer (17) and hepatocellular carcinoma (18)(19)(20)(21)(22), while it is lowly expressed in neuroblastoma (18) and prostate cancer (23). However, the biological functions and underlying mechanisms of mir-15b-5p in THca are yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑15b‑5p exerts its tumor repressive role via targeting GDI2: A novel insight into the pathogenesis of thyroid carcinoma

Zou

Qian²,

et al. 2020

Mol Med Rep

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Thyroid carcinoma (THca) is a malignant tumor of the endocrine system. Previous studies have revealed the vital roles of micrornas (mirnas/mirs) in THca procession. The present study aimed to explore the effects of mir-15b-5p on the progression of THca and its targeting mechanism. The data of THCA and healthy samples were firstly collected from starbase2.0 and used to analyze the relationship of mir-15b-5p with THca. dual-luciferase assay was performed to detect the direct interaction between mir-15b-5p and the predicted target gene GdP dissociation inhibitor 2 (Gdi2). The effects of mir-15b-5p and Gdi2 on the overall survival of patients with THca were analyzed using Kaplan-Meier analysis with log rank test. cell counting Kit-8 and Transwell assays were conducted to assess the impacts of mir-15b-5p and Gdi2 on the proliferation and invasion of THca cells. reverse transcription-quantitative Pcr and western blot analyses were performed to analyze the expression levels of the related mirnas and proteins, respectively. mir-15b-5p was found to be downregulated both in THca tissues and cells, and the low expression of mir-15b-5p was associated with the short overall survival time of patients. Moreover, the upregulation or downregulation of mir-15b-5p could inhibit or enhance the proliferation and invasion of THca cells, respectively. mir-15b-5p reduced the protein expression levels of matrix metalloproteinase (MMP)2 and MMP9, which were related to cell invasion. Furthermore, Gdi2, which was enhanced in THca and related to the poor prognosis of patients with THCA, was identified as the target gene of miR-15b-5p and negatively regulated by mir-15b-5p. additional experiments demonstrated that GDI2 overexpression could significantly reduce the antitumor effect of mir-15b-5p and its inhibitory action on the expression levels of MMP2 and MMP9. Thus, the results indicated a potential tumor suppressive role of mir-15b-5p in THca, which was mainly exerted by targeting GDI2 and modulating MMP2 and MMP9. These findings will increase the understanding on the pathogenesis of THca and provide novel candidates for THca therapy.

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miR‐15a‐5p, miR‐15b‐5p, and miR‐16‐5p inhibit tumor progression by directly targeting MYCN in neuroblastoma

Cited by 106 publications

References 70 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

KIF9‑AS1 promotes nasopharyngeal carcinoma progression by suppressing miR‑16

MicroRNA‑15b‑5p exerts its tumor repressive role via targeting GDI2: A novel insight into the pathogenesis of thyroid carcinoma

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