miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

Lv, Mingqi; Zhang, Xiaoping; Li, Maoquan; Chen, Quanchi; Ye, Meng; Liang, Wenqing; Ding, Lanbao; Cai, Haidong; Fu, Da; Lv, Zhongwei

doi:10.1371/journal.pone.0067591

Cited by 36 publications

(35 citation statements)

References 23 publications

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“…MiR26 has been shown to function as a tumor suppressor miRNA by targeting multiple genes, including EZH2 in nasopharyngeal carcinoma (35), Burkitt lymphoma (36), and lung cancer (37), IL6 in hepatocellular carcinoma (38), and CKS2 in papillary thyroid carcinoma (39). In this study, we show that miR26a and miR26b also function as tumor suppressor miRNAs in lung cancer, as miR26a and miR26b were significantly downregulated in lung cancer specimens compared with the paired normal tissues and miR26a and miR26b mimics inhibited the proliferation, migration, and invasion of lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

Zhang

Xiao

Wang

et al. 2014

Molecular Cancer Research

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Cancer is characterized by mutations, genome rearrangements, epigenetic changes, and altered gene expression that enhance cell proliferation, invasion, and metastasis. To accommodate deregulated cellular proliferation, many DNA replication-initiation proteins are overexpressed in human cancers. However, the mechanism that represses the expression of these proteins in normal cells and the cellular changes that result in their overexpression are largely unknown. One possible mechanism is through miRNA expression differences. Here, it is demonstrated that miR26a and miR26b inhibit replication licensing and the proliferation, migration, and invasion of lung cancer cells by targeting CDC6. Importantly, miR26a/b expression is significantly decreased in human lung cancer tissue specimens compared with the paired adjacent normal tissues, and miR26a/b downregulation and the consequential upregulation of CDC6 are associated with poorer prognosis of patients with lung cancer. These results indicate that miR26a/b repress replication licensing and tumorigenesis by targeting CDC6. Implications:The current study suggests that miR26a, miR26b, and CDC6 and factors regulating their expression represent potential cancer diagnostic and prognostic markers as well as anticancer targets.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

Zhang

Xiao

Wang

et al. 2014

Molecular Cancer Research

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“…For instance, microRNAs function throughout post-transcriptional gene silencing by modulating the translation of mRNAs into proteins (29) and there are recent reports on epigenetic regulation by noncoding RNAs (30). Indeed, Lv et al reported that miR26a targets and represses CKS2 expression in papillary thyroid carcinoma (31).…”

Section: Discussionmentioning

confidence: 99%

Clinical and biological impact of cyclin-dependent kinase subunit 2 in esophageal squamous cell carcinoma

et al. 2014

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Abstract. Cyclin-dependent kinase subunit 2 (CKS2) is a cyclin-dependent kinase subunit (CKS) family member that participates in cell cycle regulation. Few studies have investigated its involvement in esophageal squamous cell carcinoma (ESCC). The aim of the present study was to assess the clinical significance of CKS2 in ESCC. We used immunohistochemistry to study the clinicopathologic significance of CKS2 protein expression in 121 patients with ESCC. Using real-time reverse transcriptase-polymerase chain reaction (RT-PCR), we examined the expression of CKS2 mRNA in tumors and the corresponding normal esophageal tissues that were obtained from 62 patients. Finally, siRNA-mediated attenuation of CKS2 expression was examined in vitro. CKS2 protein expression was significantly correlated with depth of tumor invasion, clinical stage, lymphatic invasion and distant metastasis (p=0.033, 0.028, 0.041 and 0.009, respectively). CKS2 mRNA expression was higher in cancer tissue than in corresponding normal tissue (p<0.001). Patients with positive-CKS2 protein expression had a poorer five year survival frequency than patients who did not express CKS2 protein (p=0.025). In vitro, siRNA-mediated suppression of CKS2 slowed the growth rate of ESCC cells compared to control cells (p<0.001). The evaluation of CKS2 expression is useful for predicting the cause of malignant tumors and the prognosis of patients with ESSC.

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“…In certain studies, a variety of results indicated that CKS2 is a direct target of specific genes. (35) explored the miR-26a-regulated target gene(s), using three publicly-available miRNA target prediction tools: TargetScan, ncRNA and mirecords. CKS2 was selected as a potential target.…”

Section: Cks2 Acts As a Target Genementioning

confidence: 99%

CKS2 in human cancers: Clinical roles and current perspectives (Review)

You

Lin

Zhang

2015

Molecular and Clinical Oncology

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Abstract. Cyclin-dependent kinase subunit 2 (CKS2) is indicated in the processes of cell cycle and cell proliferation. Through these processes, CKS2 is identified as a cancer gene, but its role has not been well reviewed. The aim of the present study was to summarize the clinicopathological significance and the molecular mechanisms of CKS2 in human cancers. Its expression was upregulated in the majority of the types of cancer studied. CKS2 was shown to have a function in cancers of the digestive tract, genital tract, thyroid, nerve and certain other types of cancer. CKS2 can promote progression of certain cancers via positive control of proliferation, invasion and migration. Downregulation of CKS2 induces cancer cell apoptosis. CKS2 can change a multitude of cellular mechanisms in cancer pathogenesis by regulating the gene translation of numerous validated targets, such as p53, CDK1, cyclin A, cyclin B1, caspase-3 and Bax. In addition, the molecular mechanism that causes aberrant expression of CKS2 was epigenetic modification of miR-26a and the Y-box-binding protein 1 (YB-1) gene. In conclusion, CKS2 is commonly elevated in cancer, most likely due to its ability to promote cancer cell growth, invasion and migration through regulating certain significant genes. Understanding the mechanisms by which CKS2 is involved with cancer pathogenesis will be useful in the development of tumor therapy for patients with cancer.

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miR-26a and its Target CKS2 Modulate Cell Growth and Tumorigenesis of Papillary Thyroid Carcinoma

Cited by 36 publications

References 23 publications

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

MicroRNA-26a/b Regulate DNA Replication Licensing, Tumorigenesis, and Prognosis by Targeting CDC6 in Lung Cancer

Clinical and biological impact of cyclin-dependent kinase subunit 2 in esophageal squamous cell carcinoma

CKS2 in human cancers: Clinical roles and current perspectives (Review)

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