Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Wang, Xin; Zhang, Hao-Min; Jiao, Kai; Zhao, Chunyang; Liu, Hailong; Meng, Qinghong; Wang, Zhao; Feng, Chunling; Li, Yuanchun

doi:10.3892/ol.2020.11275

Cited by 8 publications

(8 citation statements)

References 26 publications

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“…The pivotal role of miR-205 in cancer is strongly suggested by our bioinformatic analysis that revealed several processes related to cancer. It is further supported by previous studies where the expression of miR-205 was confirmed to be altered in breast, endometrial, prostate, lung, bladder, thyroid, and colorectal cancer [16][17][18][19][20][21][22][23]. The relatively high basal expression of miR-205 in ovarian cell lines suggests its high biological relevance in ovarian tumors.…”

Section: Discussionsupporting

confidence: 80%

Comparative Analysis of Cell-Free miR-205-5p, let-7f-5p, and miR-483-5p Expression in Ovarian Cell Cultures and Plasma Samples of Patients with Ovarian Cancer

et al. 2021

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The term liquid biopsy reveals a non-invasive diagnostic method that might be based on the quantification of cell-free microRNAs in body fluids. However, the identification of candidates for liquid biopsy is challenging. Our aim was to compare the cell-free expression of miR-483-5p, miR-205-5p, and let-7f-5p in ovarian cell cultures and plasma samples of patients with ovarian cancer. Both the intracellular and cell-free expression of miR-205-5p and let-7f-5p proved to be higher in the Estrogen Receptor α (ERα) expressing PEO1 cell-line than in the estrogen non-sensitive A2780. Moreover, the expression of let-7f-5p was up-regulated in response to estradiol exposure that was diminished after the addition of an ERα selective antagonist. MiR-483-5p had lower intracellular and cell-free expression in PEO1. All these miRNAs had detectable expression level in plasma samples, among which miR-205-5p proved to be overexpressed in the plasma samples of patients with ovarian tumors compared to healthy controls and possessed an acceptable diagnostic potential with ROC-AUC 0.683 (95% CI 0.57–0.795). Functional annotation clustering of the target genes of miR-205-5p revealed several clusters involved in cancer development. We suggest that miR-205-5p might be a promising biomarker candidate in ovarian cancer that should be further analyzed in larger sample size.

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Section: Discussionsupporting

confidence: 80%

Comparative Analysis of Cell-Free miR-205-5p, let-7f-5p, and miR-483-5p Expression in Ovarian Cell Cultures and Plasma Samples of Patients with Ovarian Cancer

et al. 2021

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“…And the abnormal expression of cyclin B2 is related to the cell cycle regulation disorder, also triggering cell malignant transformation. 29 This study revealed that NUCKS1 overexpression upregulated the expression of CDK1, cyclin A2, cyclin B1 and cyclin B2 in both A549 and NCI-H460 cells. Following transfection with CDK1 or treatment with CDK1 inhibitor p2767-00, the impact of NUCKS1 overexpression on proliferation, invasion and migration of NSCLC cells was remarkably reversed.…”

Section: Discussionmentioning

confidence: 66%

NUCKS1 Promotes Proliferation, Invasion and Migration of Non-Small Cell Lung Cancer by Upregulating CDK1 Expression

Zhao

Wang

et al. 2020

CMAR

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Background Non-small cell lung cancer (NSCLC) is a predominant type of lung cancer with a high mortality rate. Objective The aim of this study is to investigate the roles of nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) in NSCLC and to identify the potential mechanisms. Materials and Methods The expression of NUCKS1 in several NSCLC cells was detected firstly. Then, NUCKS1 was overexpressed or silenced in both A549 and NCI-H460 cells, where cell proliferation, invasion and migration were, respectively, determined, using CCK-8, colony formation assay, transwell and wound healing assays. Cell cycle analysis was performed, and the expression-associated proteins were detected by Western blotting. Subsequently, NCI-H460 cells with NUCKS1 overexpression for the subsequent tumor-bearing experiment. And the NUCKS1 expression in tumor tissues was measured by means of immunohistochemistry and Western blotting. Additionally, the STRING database predicted that Cyclin-Dependent Kinase 1 (CDK1) would bind to NUSK1, which was verified by the co-immunoprecipitation assay. Then, CDK1 was silenced by transfection with short hairpin RNA (shRNA)-CDK-1 or by exposure to CDK1 inhibitor p2767-00. And the biological characteristics of proliferation, invasion and migration were examined. Results Results indicated that NUCKS1 was overly expressed in NSCLC cells, and its overexpression promoted proliferation, invasion and migration of both A549 and NCI-H460 cells while NUCKS1 knockdown displayed the opposite effects. Moreover, the results of the xenograft experiments revealed that NUCKS1-upregulation promoted the tumor growth. Furthermore, the immunoprecipitation assay verified CDK1’s interaction with NUCKS1, and CDK1 knockdown alleviates the impact of NUCKS1 overexpression on NSCLC cell proliferation, invasion and migration. Conclusion Taken together, these findings demonstrated that NUCKS1 promotes proliferation, invasion and migration of NSCLC by upregulating CDK1, providing a novel putative target for the clinical treatment of NSCLC.

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“…As previously noted in a series of reports, besides the classic oncogenes like BRAF or RET, dysregulation of miRs is implicated in the tumorigenicity and progression of PTC ( 21 ). Among them, miR-205-5p has been proposed to exert tumor suppressor functions via repression of the downstream target gene expression, such as YAP1 ( 33 ), VEGFA ( 22 ), and CCNB2 ( 34 ). In this study, we revealed GGCT is a novel target gene of miR-205-5p through the dual-luciferase reporter and RNA-RNA pull-down assays.…”

Section: Discussionmentioning

confidence: 99%

MiR-205-5p/GGCT Attenuates Growth and Metastasis of Papillary Thyroid Cancer by Regulating CD44

Zhang

et al. 2022

Endocrinology

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Papillary thyroid cancer (PTC) is the most common endocrine malignancy, despite marked achieves in recent decades, the mechanisms underlying the pathogenesis and progression for PTC are incomplete. Accumulating evidence show that γ-glutamylcyclotransferase (GGCT), an enzyme participated in glutathione homeostasis that is elevated in multiple types of tumors, represents an attractive therapeutic target. Using bioinformatics, immunohistochemistry, qRT-PCR and western blot assays, we found that GGCT expression was upregulated in PTC, correlated with more aggressive clinicopathological characteristics and worse prognosis. GGCT knockdown inhibited the growth and metastasis ability of PTC cells both in vitro and in vivo and reduced the expression of mesenchymal markers (N-cadherin, CD44, MMP2 and MMP9) while increased epithelial marker (E-cadherin) in PTC cells. We confirmed binding of miR-205-5p on the 3’-UTR regions of GGCT by dual luciferase reporter assay, RNA-RNA pull down assay. Delivery of miR-205-5p reversed the pro-malignant capacity of GGCT both in vitro and in vivo. Lastly, we found GGCT interacted with and stabilized CD44 in PTC cells by co-immunoprecipitation and immunohistochemistry assays. Our findings illustrate a novel signaling pathway, miR-205-5p/GGCT/CD44, that involves in the carcinogenesis and progression of PTC. Development of miR-205-mimics or GGCT inhibitors as potential therapeutics for PTC may have remarkable applications.

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Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Cited by 8 publications

References 26 publications

Comparative Analysis of Cell-Free miR-205-5p, let-7f-5p, and miR-483-5p Expression in Ovarian Cell Cultures and Plasma Samples of Patients with Ovarian Cancer

Comparative Analysis of Cell-Free miR-205-5p, let-7f-5p, and miR-483-5p Expression in Ovarian Cell Cultures and Plasma Samples of Patients with Ovarian Cancer

NUCKS1 Promotes Proliferation, Invasion and Migration of Non-Small Cell Lung Cancer by Upregulating CDK1 Expression

MiR-205-5p/GGCT Attenuates Growth and Metastasis of Papillary Thyroid Cancer by Regulating CD44

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