MicroRNAs contribute to the chemoresistance of cisplatin in tongue squamous cell carcinoma lines

Yu, Zhiwei; Zhong, Lai‐ping; Ji, Tong; Zhang, Ping; Chen, Wantao; Zhang, Chenping

doi:10.1016/j.oraloncology.2010.02.002

Cited by 117 publications

(102 citation statements)

References 20 publications

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“…Moreover, we also observed elevated expression levels of miR-214 in oral cancer tissues, consistent with another study (Scapoli et al, 2010). Unsurprisingly, miR-214 levels were reported to be significantly elevated in cisplatin resistant tongue squamous carcinoma cell line Tca/cisplatin compared to those in cisplatin sensitive Tca8113, indicating the role of miR-214 in tumor promotion in oral cancer (Yu et al, 2010).…”

Section: Discussionsupporting

confidence: 91%

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

Yin

Chen

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Ras association domain family member 5 (RASSF5), a member of the Ras association domain family, induces cell apoptosis by phosphorylating FOXO3a, which triggers target gene BIM (proapoptotic factor) activation. MiR-214 is overexpressed in oral cancer tissue, indicating its possible involvement in oral cancer pathogenesis. Bioinformatics analysis has revealed a complimentary sequence between miR-214 and the 3'-UTR of RASSF5 mRNA. However, whether miR-124 regulates RASSF5 in oral cancer remains poorly understood. We aimed to investigate the role of miR-214 in RASSF5 expression regulation in oral cancer. Tumor and paracarcinoma tissues were obtained from 48 oral cancer patients to examine miR-214 and RASSF5 expression. The relationship between miR-214 and RASSF5 was investigated by dual luciferase reporter gene assay. Oral cancer KB cells were cultured in vitro and divided into inhibitor NC, miR-214 inhibitor, Scramble-pMD18, RASSF5-pMD18, and miR-214 inhibitor + RASSF5-pMD18 groups. Caspase 3 activity, cell apoptosis, and total protein expression were measured by spectrophotometry, flow cytometry, and western blot, respectively. MiR-214 expression was significantly increased, while that of RASSF5 decreased in oral cancer tumor tissues compared to paracarcinoma tissues. Luciferase assay showed that miR-214 suppressed RASSF5 expression by targeting its 3'-UTR. Down-regulation of miR-214 and/or enhancement of RASSF5 expression markedly increased FOXO3a phosphorylation, BIM expression, caspase 3 activity, and apoptosis. In conclusion, miR-214 expression was elevated and RASSF5 was down-regulated in oral cancer. Moreover, miR-214 regulated KB cell apoptosis through targeted inhibition of RASSF5 expression, FOXO3a phosphorylation, and BIM expression, suggesting its possible application as a novel therapeutic oral cancer target.

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Section: Discussionsupporting

confidence: 91%

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

Yin

Chen

et al. 2017

Genet. Mol. Res.

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“…miR-214 is increased in many cancers, including pancreatic cancer, oral squamous cell carcinoma, and malignant melanoma (69 -71). In tongue squamous cell carcinoma and ovarian cancer, enhanced expression of miR-214 is associated with cisplatin resistance (72,73). Although aberrant expression of many miRNAs has been identified in RCC, we demonstrate significant down-regulation of miR-214 in VHL-positive and VHLdeficient renal cancer cells compared with normal proximal tubular epithelial cells (Fig.…”

Section: Discussionmentioning

confidence: 60%

MicroRNA-214 Reduces Insulin-like Growth Factor-1 (IGF-1) Receptor Expression and Downstream mTORC1 Signaling in Renal Carcinoma Cells

Das

Dey

Bera

et al. 2016

Journal of Biological Chemistry

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Renal cell carcinoma (RCC)5 accounts for nearly 3% of all malignancies. Among the five histologic subtypes, clear cell renal carcinoma accounts for about 85% of all RCCs (1, 2). About 30% of patients show renal cancer metastasis to lung, liver, bone, and brain at the time of diagnosis, and half of the remaining patients eventually develop metastasis (3-5). Individuals bearing germ line mutation in the von Hippel-Lindau (VHL) tumor suppressor gene located on chromosome 3p have increased risk for clear cell RCC. Inherited forms of RCC occur when the remaining wild type VHL allele is lost.Apart from inactivated VHL-driven tumorigenesis, IGF-1 signal transduction significantly contributes to the growth of RCC cells in vitro and in vivo in animal models (6, 7). In fact, increased IGF-1 mRNA and protein levels in the kidney are significantly higher in RCC in humans (8, 9). Similarly, IGF-1 receptor (IGF-1R) expression has also been shown to be significantly associated with increased risk of RCC (10, 11). Also, patients with IGF-1R-positive RCC showed significantly reduced survival rates (12, 13). The dimeric IGF-1R shares significantly high homology with insulin receptor. IGF-1R is produced as a single polypeptide, which is cleaved to form the mature ␣-and ␤-subunits. The ␣-protein represents the transmembrane protein with extracellular domain, whereas the ␤-subunit is exclusively intracellular. The IGF-1 binds to the extracellular domain of ␣-subunit, resulting in heterotetramerization. Upon ligand binding, conformational change in the juxtamembrane domain induces an increase in tyrosine kinase activity of the ␤-subunit, which autophosphorylates specific tyrosine residues in the ␤-subunit. Tyrosine-phosphorylated ␤-subunit recruits the IRS protein through binding to its N-terminal PTB domain. Receptor-bound IRS protein serves as docking sites for the Src homology 2 domain-containing proteins, which trigger signal transduction to induce tumor growth of RCC mainly by two arms, the Ras/MAPK and phosphatidylinositol 3-kinase/Akt pathways (14, 15). Because of significant homology between IGF-1R and insulin receptor, they can form a hybrid receptor, which binds IGF-1 with an affinity similar to that with IGF-1R heterotetramer alone, and can elicit mitogenic signal transduction in tumor cells (14,15). Therefore, * This work was supported in part by the Veterans Affairs Research Service Merit Review Grant 2 I01 BX000926 and National Institutes of Health Grant RO1 DK50190 (to G. G. C.). The authors declare that they have no conflicts of interest with the contents of this article. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. We dedicate this paper to Dr. Hanna E. Abboud, who unexpectedly left us on January 7, 2015. His continued encouragement and support were vital for the completion of this work. 1 Both authors contributed equally to this work. 2 Supported by Veterans Affairs Merit Review Grant 5I01BX001340. 3 Supported by V...

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“…Tongue squamous cell carcinoma (TSCC), the most common type of oral cancer, often leads to malfunctions in speech, mastication and deglutition (1). TSCC is well-known for its high rate of proliferation and nodal metastasis; metastasis is the most reliable adverse prognostic factor in TSCC patients (2).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-149 targets specificity protein 1 to suppress human tongue squamous cell carcinoma cell proliferation and motility

Chen

2016

Oncology Letters

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MicroRNAs contribute to the chemoresistance of cisplatin in tongue squamous cell carcinoma lines

Cited by 117 publications

References 20 publications

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

MiR-214 regulates oral cancer KB cell apoptosis through targeting RASSF5

MicroRNA-214 Reduces Insulin-like Growth Factor-1 (IGF-1) Receptor Expression and Downstream mTORC1 Signaling in Renal Carcinoma Cells

MicroRNA-149 targets specificity protein 1 to suppress human tongue squamous cell carcinoma cell proliferation and motility

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