Micro<scp>RNA</scp> expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

Yu, Xin; Li, Zheng

doi:10.1111/jcmm.12650

Cited by 54 publications

(50 citation statements)

References 59 publications

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“…Emerging evidence have confirmed the important function of microRNAs in cancer development and tumorigenesis, including TSCC, acting as potent oncogenes or tumor suppressors [19]. Dysregulated micro-RNAs are also involved in the diagnosis and cure of TSCC [20]. In our study, we validated that miR-26a/ miR-26b was downregulated in TSCC tumor tissues and cells, which was similar to former reports [11,12].…”

Section: Discussionsupporting

confidence: 91%

MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1

et al. 2020

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Background: Tongue squamous cell carcinoma (TSCC) is the most common oral malignancy. Previous studies found that microRNA (miR)-26a and miR-26b were downregulated in TSCC tissues. The current study was designed to explore the effects of miR-26a/miR-26b on TSCC progression and the potential mechanism. Methods: Expression of miR-26a, miR-26b and p21 Activated Kinase 1 (PAK1) in TSCC tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Flow cytometry analysis was performed to examine cell cycle and apoptosis. Transwell assay was conducted to evaluate the migrated and invasive abilities of SCC4 and Cal27 cells. In addition, western blot assay was employed to analyze the protein level. Glucose assay kit and lactate assay kit were utilized to analyze glycolysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to explore the relationship between miR-26a/miR-26b and PAK1. Xenograft tumor model was constructed to explore the role of miR-26a/miR-26b in vivo. Results: Both miR-26a and miR-26b were underexpressed, while PAK1 was highly enriched in TSCC. Overexpression of miR-26a and miR-26b inhibited TSCC cell cycle, migration invasion and glycolysis, while promoted cell apoptosis. Both miR-26a and miR-26b directly targeted and negatively regulated PAK1 expression. Introduction of PAK1 partially reversed miR-26a/miR-26b upregulation-mediated cellular behaviors in TSCC cells. Gain of miR-26a/miR-26b blocked TSCC tumor growth in vivo. Conclusion: MiR-26a/miR-26b repressed TSCC progression via targeting PAK1 in vitro and in vivo, which enriched our understanding about TSCC development and provided new insights into the its treatment.

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Section: Discussionsupporting

confidence: 91%

MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1

et al. 2020

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“…20 It is well recognized that miRNA is a post-transcriptional regulator by decreasing mRNA stability or inhibiting translation via directly targeting gene 3′-UTR. 21 In the current study, we identified that circ-CCND1 could simultaneously sponge three miR-646 to diminish the repression of miR-646 on CCND1 3′-UTR, resulting in enhancing the stability of CCND1 mRNA. Growing evidence indicates that miR-646 plays a tumour-suppressive role in a variety of human cancers, including osteosarcoma, 22 hepatocellular carcinoma 23 and gastric cancer.…”

Section: Discussionmentioning

confidence: 66%

“…The most extensively studied is circRNA as a competing endogenous RNA (ceRNA) to effectively sponge miRNA, for example, circ‐HIPK3/miR‐7 in colorectal cancer, circ‐EPSTI1/miR‐942 in ovarian cancer, circ‐ANKS1B/miR‐148/152 in breast cancer and circ‐AMOTL1L/miR‐193a‐5p in prostate cancer . It is well recognized that miRNA is a post‐transcriptional regulator by decreasing mRNA stability or inhibiting translation via directly targeting gene 3′‐UTR . In the current study, we identified that circ‐CCND1 could simultaneously sponge three miR‐646 to diminish the repression of miR‐646 on CCND1 3′‐UTR, resulting in enhancing the stability of CCND1 mRNA.…”

Section: Discussionmentioning

confidence: 99%

circRNA circ‐CCND1 promotes the proliferation of laryngeal squamous cell carcinoma through elevating CCND1 expression via interacting with HuR and miR‐646

Zang

Wan

et al. 2020

J Cellular Molecular Medi

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Cyclin D1 (CCND1) is a well‐known proliferation promoter that accelerates G1/S transition in cancer. However, the underlying mechanism by which CCND1 is regulated is still largely unknown. In this study, we identified a novel circular RNA (circRNA) derived from CCND1 (circ‐CCND1, hsa_circ_0023303) as a key regulator for CCND1. circ‐CCND1 was found to be markedly up‐regulated in laryngeal squamous cell carcinoma (LSCC) and closely associated with aggressive clinical features and adverse prognosis. Depletion of circ‐CCND1 significantly inhibited LSCC cell proliferation in vitro and retarded tumour growth in vivo. Regarding the mechanism, circ‐CCND1 physically bound to human antigen R (HuR) protein to enhance CCND1 mRNA stability; on the other hand, circ‐CCND1 could act as an effective sponge for miR‐646 to alleviate the repression of miR‐646 on CCND1 mRNA. As a result, circ‐CCND1 post‐transcriptionally elevated CCND1 expression via coordinated avoidance of CCND1 mRNA decay, thereby promoting LSCC tumorigenesis. Taken together, our findings uncover the essential proliferation‐promoting role of circ‐CCND1 through regulation of the stability of CCND1 mRNA in LSCC. Targeting circ‐CCND1 may be a promising treatment for LSCC patients.

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“…MicroRNAs (miRNAs) are small noncoding RNAs that can suppress the expression of protein coding genes by targeting mRNAs for cleavage and/or translational repression [13][14][15][16]. Recent evidence has demonstrated that miRNAs play critical roles in many biological processes, such as lineage determination and cell proliferation, migration, apoptosis and differentiation [2,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Retracted: MicroRNA‑224 promotes the sensitivity of osteosarcoma cells to cisplatin by targeting Rac1

Geng

Fang

et al. 2016

J Cellular Molecular Medi

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Osteosarcoma is the most common primary bone tumour in children and adolescents. Accumulating evidence has shown that microRNAs (miRNAs) participate in the development of almost all types of cancer. Here, we investigated the role of miR‐224 in the development and progression of osteosarcoma. We demonstrated that miR‐224 was down‐regulated in osteosarcoma cell lines and tissues. Lower miR‐224 levels were correlated with shorter survivalin osteosarcoma patients. Furthermore, overexpression of miR‐224 suppressed osteosarcoma cell proliferation, migration and invasion and contributed to the increased sensitivity of MG‐63 cells to cisplatin. We identified Rac1 as a direct target gene of miR‐224 in osteosarcoma. Rac1 expression was up‐regulated in the osteosarcoma cell lines and tissues, and there was an inverse correlation between Rac1 and miR‐224 expression in osteosarcoma tissues. Furthermore, rescuing Rac1 expression decreased the sensitivity of miR‐224‐overexpressing MG‐63 cells to cisplatin. We also demonstrated that ectopic expression of Rac1 promoted the proliferation, migration and invasion of miR‐224‐overexpressing MG‐63 cells. These data suggest that miR‐224 plays a tumour suppressor role in the development of osteosarcoma and is related to the sensitivity of osteosarcoma to cisplatin.

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MicroRNA expression and its implications for diagnosis and therapy of tongue squamous cell carcinoma

Cited by 54 publications

References 59 publications

MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1

MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1

circRNA circ‐CCND1 promotes the proliferation of laryngeal squamous cell carcinoma through elevating CCND1 expression via interacting with HuR and miR‐646

Retracted: MicroRNA‑224 promotes the sensitivity of osteosarcoma cells to cisplatin by targeting Rac1

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