Inhibition of NOB1 by microRNA-330-5p overexpression represses cell growth of non-small cell lung cancer

Kong, Ranran; Liu, Wei; Guo, Yurui; Feng, Jie; Cheng, Chuantao; Zhang, Xinwu; Ma, Yuefeng; Li, Shaomin; Jiang, Jiantao; Zhang, Jin; Qiao, Zhe; Qin, Jie; Lu, Taihe; He, Xijing

doi:10.3892/or.2017.5927

Cited by 26 publications

(21 citation statements)

References 49 publications

(60 reference statements)

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“…16 MiRNA (miR)-330-5p is downregulated in multiple malignant tumors, such as glioblastoma, colorectal cancer, prostate cancer, [17][18][19] and NSCLC as well. 20 The 3-phosphoinositide-dependent protein kinase-1 (PDK1), one crucial node of the PI3K pathway, can physically phosphorylate AKT. 21 Moreover, PDK1 is a key oncogene to promote NSCLC cell growth and metastasis.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of circPRKCA Restrained Cell Growth, Migration, and Invasion of NSCLC Cells Both in vitro and in vivo via Regulating miR-330-5p/PDK1/AKT Pathway

Bai¹,

Peng²,

Sun³

2020

CMAR

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Background: Protein kinase Cα (PRKCA) is an oncogene in multiple cancers including non-small-cell lung cancer (NSCLC) and can be transcribed into a number of circular PRKCAs (circPRKCAs). Here, we aimed to elaborate the role and mechanism of circPRKCA_024 (circPRKCA) in malignant progression of NSCLC. Methods: Expression of circPRKCA, miRNA (miR)-330-5p and 3-phosphoinositidedependent protein kinase-1 (PDK1) was measured by real-time quantitative PCR and Western blotting, and their relationship was testified by dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. Cell behaviors were evaluated by cell counting kit (CCK)-8, flow cytometry, and transwell assays. AKT activity was confirmed by Western blotting. Xenograft experiment assessed tumor growth. Results: Expression of circPRKCA and PDK1 was upregulated, and miR-330-5p was downregulated in NSCLC tissues and cell lines. High circPRKCA was correlated with TNM stage and lymph node metastasis of NSCLC patients. Silencing circPRKCA could suppress cell viability, migration, and invasion in A549 and H1299 cells, accompanied with apoptosis rate promotion. Moreover, circPRKCA knockdown retarded tumor growth of A549 cells in vivo. Molecularly, miR-330-5p was sponged by circPRKCA, and PDK1 was a target of miR-330-5p. Inhibiting miR-330-5p could attenuate the suppression of circPRKCA knockdown on cell growth, migration, and invasion; contrarily, promoting miR-330-5p caused inhibition on those cell behaviors by downregulating PDK1. Analogously, AKT activity was suppressed by circPRKCA downregulation and miR-330-5p upregulation in NSCLC cells both in vitro and in vivo. Conclusion: Depleting circPRKCA inhibited PDK1 to suppress NSCLC cell malignant behaviors through miR-330-5p/PDK1/AKT pathway.

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Section: Introductionmentioning

confidence: 99%

Knockdown of circPRKCA Restrained Cell Growth, Migration, and Invasion of NSCLC Cells Both in vitro and in vivo via Regulating miR-330-5p/PDK1/AKT Pathway

Bai¹,

Peng²,

Sun³

2020

CMAR

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“…The mutant sequence of miR-330 is miR-330-5p, and several studies reported that miR-330-5p unction as oncogenes or tumor suppressor genes in tumor progression such as breast cancer, lung cancer, prostate cancer, PC, etc. [28][29][30][31] MiRNAs can regulate tumorogenesis by regulating their target mRNAs, and miR-330-5p directly bound to RASSF1 3′-UTR. Recent evidence indicated that RASSF1 is involved in various biological processes such as apoptotic signaling, microtubule stabilization, and mitotic progression, etc.…”

Section: Discussionmentioning

confidence: 99%

CircHIPK3 Promotes Gemcitabine (GEM) Resistance in Pancreatic Cancer Cells by Sponging miR-330-5p and Targets RASSF1

Liu¹,

Li²,

Luo³

et al. 2020

CMAR

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Background: Pancreatic cancer is one of the most common malignant diseases in the world. Gemcitabine chemotherapy remains the most important clinical treatment. However, research found that pancreatic cancer cells have chemoresistance to gemcitabine and the effect is not satisfactory. Therefore, it is urgent to find an effective early diagnosis and treatment strategy. Circular RNA is one of the most popular prognostic biomarkers in GEM-resistant PC. Materials and Methods: The present study was designed to evaluate the role of circHIPK3 in PC. The expression of circHIPK3 in PC tissues and cells and its effect on proliferation, migration, invasion, EMT, and apoptosis were investigated in vitro; its effect on tumor xenografts was assessed in vivo. Used bioinformation analysis to predict which miRNAs could potentially interact with circHIPK3, mRNA, and miR-330-5p. Results: RT-PCR showed that the level of circHIPK3 was increased in PC tumor tissues; moreover, circHIPK3 was also increased in GEM-resistant PC tumors tissues and GEMresistant PC cells. Sh-circHIPK3 could knockdown circHIPK3 in PANC-1-GEM and SW-1990-GEM and could significantly inhibit cell proliferation, invasion, migration, EMT and enhance cell apoptosis, compare with control group, the tumor xenografts of circHIPK3 knockdown group were significantly smaller. CircHIPK3 served as a sponge for miR-330-5p, and miR-330-5p directly bound to the 3′ UTR of RASSF1 were revealed by dual luciferase assay and RIP in PC cells. CircHIPK3 knockdown of RASSF1 expression could neutralize the cytological function of PC cells by miR-330-5p inhibitor mediated GEM-resistance. Conclusion: CircHIPK3 promotes gemcitabine (GEM) resistance in pancreatic cancer cells by targeting RASSF1 via miR-330-5p and regulates proliferation, invasive, migration, EMT, and apoptosis. Our research revealed that circHIPK3 may be a novel biomarker in GEMresistant PC and could be used as a prognostic target.

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“…NOB1 could cleave RNA substrate that contains the D site of pro-ribosomal RNA, thereby regulating protease functions and RNA metabolism [16]. NOB1 acted as an oncogene and was upregulated in a variety of cancers that include cervical cancer, gastric cancer, epithelial ovarian cancer, and non-small cell lung cancer [18][19][20][21]. Silencing of NOB1 could inhibit cell growth and metastasis of laryngeal cancer and colorectal cancer [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…The RNA substrate containing the D site of pro-ribosomal RNA is efficiently cleaved by NOB1 in a manganese-dependent manner, thereby regulating protease function and RNA metabolism [17]. NOB1 was upregulated and acted as an oncogene in a variety of cancers including cervical cancer, gastric cancer, epithelial ovarian cancer, and non-small cell lung cancer [18][19][20][21]. In laryngeal cancer, Gao et al have discovered that silencing of NOB1 could inhibit cell growth and metastasis [22].…”

Section: Introductionmentioning

confidence: 99%

MiR-363 suppresses cell migration, invasion, and epithelial-mesenchymal transition of osteosarcoma by binding to NOB1

Wang

Zhang

2020

World J Surg Onc

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Background: Osteosarcoma (OS) is a primary malignant bone tumor with a high rate of metastasis and a short 5year survival rate. MiR-363 was downregulated in a variety of tumors and played a role in suppressing tumors. However, the roles of miR-363 in osteosarcoma remain unknown; thus, the purpose of this study was to explore the functions of miR-363 in osteosarcoma. Methods: CCK-8 and transwell assays were performed to evaluate the proliferation, migration, and invasion abilities of MG63 cells. The epithelial-mesenchymal transition (EMT) and apoptosis-associated proteins were measured by using Western blot assay. Luciferase reporter assay was utilized to verify whether miR-363 directly bound to the 3′-UTR of NOB1 mRNA. Results: MiR-363 was downregulated while NOB1 was upregulated in osteosarcoma clinical tissue specimens and cell lines as compared with the adjacent normal tissue specimens and normal cell line. The miR-363 is reversely correlated with the expression of NOB1 in osteosarcoma tissues. Overexpression of miR-363 suppressed the ability of cell migration, invasion, and EMT, whereas low expression of miR-363 promoted this ability. In addition, miR-363 inhibited osteosarcoma proliferation both in vitro and in vivo and inhibited the apoptosis in MG63 cells. Interference of NOB1 could inhibit the migration, invasion, and EMT of osteosarcoma cell line MG63. NOB1 was verified to be a direct target of miR-363 and its expression was mediated by miR-363. Re-expression of NOB1 could partially reverse the inhibitory effect of miR-363 on cell migration and invasion. In addition, low expression of miR-363 or overexpression of NOB1 predicted poor prognosis of osteosarcoma patients. Conclusion: MiR-363 inhibited osteosarcoma the proliferation, migration, invasion, and EMT and induced the apoptosis by directly targeting NOB1 in MG63 cells. The newly identified miR-363/NOB1 axis provides novel insights into the pathogenesis of osteosarcoma.

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Inhibition of NOB1 by microRNA-330-5p overexpression represses cell growth of non-small cell lung cancer

Cited by 26 publications

References 49 publications

<p>Knockdown of circPRKCA Restrained Cell Growth, Migration, and Invasion of NSCLC Cells Both in vitro and in vivo via Regulating miR-330-5p/PDK1/AKT Pathway</p>

<p>Knockdown of circPRKCA Restrained Cell Growth, Migration, and Invasion of NSCLC Cells Both in vitro and in vivo via Regulating miR-330-5p/PDK1/AKT Pathway</p>

<p>CircHIPK3 Promotes Gemcitabine (GEM) Resistance in Pancreatic Cancer Cells by Sponging miR-330-5p and Targets RASSF1</p>

MiR-363 suppresses cell migration, invasion, and epithelial-mesenchymal transition of osteosarcoma by binding to NOB1

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