Micro<scp>RNA</scp>‐26a inhibits proliferation and tumorigenesis via targeting <scp>CKS</scp>2 in laryngeal squamous cell carcinoma

Wu, Zhiyan; Lu, Baocai; Li, Xiao; Miao, Wenjie; Li, Jin; Shi, Yongjuan; Yu, Wenfa

doi:10.1111/1440-1681.12890

Cited by 15 publications

(12 citation statements)

References 35 publications

(65 reference statements)

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“…From The Cancer Genome Atlas (TCGA) database, a number of differentially expressed miRNAs in LSCC have been identified [11]. Several miRNAs, including miR-26a and miR-153, emerged as powerful regulators in LSCC, as indicated in recent studies [12,13]. One major finding of our study is that miR-625 was markedly decreased in LSCC tissue specimens and cell lines.…”

Section: Discussionsupporting

confidence: 52%

MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

Tao

Dai

et al. 2019

Bioscience Reports

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Introduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.

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Section: Discussionsupporting

confidence: 52%

MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

Tao

Dai

et al. 2019

Bioscience Reports

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“…The miRNA‐26a mimic and a negative control of miRNA‐26a mimic (mi‐NC) were purchased from Ambion (Carlsbad, California). LP1 and U266 cells were transfected with miRNA‐26a mimic or mi‐NC for 3 days by Lipofectamine RNAiMAX Reagent (Invitrogen) in Opti‐MEM medium (Invitrogen) according to the manufacturer's instruction as described previously …”

Section: Methodsmentioning

confidence: 99%

“…LP1 and U266 cells were transfected with miRNA-26a mimic or mi-NC for 3 days by Lipofectamine RNAiMAX Reagent (Invitrogen) in Opti-MEM medium (Invitrogen) according to the manufacturer's instruction as described previously. 13 Human CDK6 editing sequences were amplified by PCR, and were cloned into the lentiviral vector pCDH-CMV-MCS-EF1-copGFP at unique EcoRI and BamHI sites. Lentiviral particles were produced in HEK293T cells and infected LP1 cells.…”

Section: Mirna Transfection and Lentivirus Infectionmentioning

confidence: 99%

MicroRNA‐26a inhibits multiple myeloma cell growth by suppressing cyclin‐dependent kinase 6 expression

Song

Huang

et al. 2019

The Kaohsiung J of Med Scie

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MicroRNA‐26a (miR‐26a) has been reported to be involved in the tumorigenesis of several tumors, but its biological function and molecular mechanism in multiple myeloma (MM) are still unknown. In this study, we found that overexpression of miR‐26a obviously inhibited MM cell growth, and delayed tumor growth in xenografts. Further studies showed that overexpression of miR‐26a induced cell cycle arrest at G0/G1 phase in MM cells. MiR‐26a mimic down‐regulated the expression levels of CDK6 and E2F1, but up‐regulated p53 and p21 expression. In contrast, overexpression of CDK6 decreased the effect of miR‐26a mimic on MM cell survival. Moreover, miR‐26a targeted CDK6 mRNA and thus suppressed CDK6 protein expression. Overexpression of miR‐26a also enhanced the cytotoxic action of doxorubicin against MM. These results demonstrated that miR‐26a was involved in the development of MM through regulating CDK6 signaling pathway, and indicated that miR‐26a could be as a novel target for anti‐tumor therapy in clinic as a single strategy or in combination with other anti‐tumor drugs in MM.

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“…In addition, the role of genetic factors in the pathogenesis of laryngeal cancer is also gradually recognized. While the proto-oncogene may be related to the carcinogenesis, the mutation and inactivation of tumor suppressor genes could also be prime laryngeal cancer mechanisms [7][8][9].…”

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confidence: 99%

Over-expression of MEOX2 promotes apoptosis through inhibiting the PI3K/Akt pathway in laryngeal cancer cells

Tian

Tao

et al. 2018

neo

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The early-stage diagnosis and treatment for the recurrence of larynx carcinoma needs further investigation. Mesenchyme homeobox 2 (MEOX2) was speculated as a novel suppressor gene in larynx carcinoma in our study, the molecular mechanism was studied. Real-time quantitative PCR (RT-qPCR) and Western blot were used to detect mRNA and protein levels of MEOX2 in laryngeal cancer tissues and cells (Hep-2, TU212, AMC-NH-8 and TU686 cells), and also apoptosis and phosphoinositide 3-kinase (PI3K)/protein kinase (Akt) related factors in TU212 cells transfected with MEOX2. Cell counting kit-8 (CCK8) assay and Annexin-Ⅴ/PI staining assay were conducted to determine cell viability and apoptosis rates respectively.46 patients with larynx carcinoma were involved in this study. The expression of MEOX2 was lower in larynx carcinoma tissues than normal tissues, correlated with clinical stages, differentiated degrees, and survival times. The expression of MEOX2 was the lowest among those laryngeal cancer cells, and was chosen to be transfected with MEOX2 in the following study. Over-expression of MEOX2 inhibited cell viability and promoted apoptosis of TU212 cells, via increasing the expression levels of Caspase-3, and decreasing levels of C-Myc, XIAP, PI3K p110α, PI3K p110β, PI3K class III and p-Akt. In summary, the expression levels of MEOX2 were inhibited in larynx carcinoma than normal tissues, correlated with the progression of the cancer. Over-expression of MEOX2 in laryngeal cancer cells inhibited cell viability and promoted apoptosis, via regulating apoptosis and PI3K/Akt pathway related factors. It would provide evidence for MEOX2 to be used as a therapeutical gene in larynx carcinoma.

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MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

Cited by 15 publications

References 35 publications

MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

MicroRNA-625 inhibits cell invasion and epithelial–mesenchymal transition by targeting SOX4 in laryngeal squamous cell carcinoma

MicroRNA‐26a inhibits multiple myeloma cell growth by suppressing cyclin‐dependent kinase 6 expression

Over-expression of MEOX2 promotes apoptosis through inhibiting the PI3K/Akt pathway in laryngeal cancer cells

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