MiR-506 suppresses cell proliferation and tumor growth by targeting Rho-associated protein kinase 1 in hepatocellular carcinoma

Deng, Quanjun; Xie, Li; Li, Hua

doi:10.1016/j.bbrc.2015.10.043

Cited by 23 publications

(14 citation statements)

References 19 publications

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“…In breast cancer cell lines, the transition between epithelial and mesenchymal cells was regulated by miR-506 [7]. It was also indicated that in hepatocellular carcinoma, miR-34a targeted the protein kinase 1 that was associated with Rho, which then suppressed the proliferation of cells and the growth of tumors [8]. In human and clinical cervical cancer cell specimens (HeLa and C33A), significant downregulation of miR-506 was reported compared to that of matched cell lines and adjacent normal tissues.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1

et al. 2019

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Previous research has shown that microRNA 506 (miR-506) functions as an essential modulator in the development of many biological reactions, including multiple cancers. However, its involvement in cutaneous squamous cell carcinoma (CSCC) has been rarely reported. In the present work, we investigated the molecular mechanism and function of miR-506 in the regulation of CSCC cell viability and metastasis (migration and invasion). We observed that miR-506 expression was upregulated in both CSCC tissues and cell lines, and that decreased miR-506 expression led to repressed tumorigenesis in CSCC cells. Furthermore, flow cytometry revealed that the depletion of miR-506 resulted in decreased proliferation and increased apoptotic levels in CSCC cells. Meanwhile, it was found that miR-506 decreased CSCC cell migration and invasion in vitro. The dual-luciferase reporter assay also revealed that miR-506 targets the 3′-UTRs of p65 and Laminin C1 (LAMC1) for silencing. Silencing of p65 expression counteracted the pro-apoptotic influence of miR-506 depletion in CSCC cells, while inhibition of LAMC1 expression restored the migration and invasion properties of the CSCC cells. Therefore, the results provide evidence for the need to probe the biological and molecular mechanisms behind the development and progression of CSCC and may lead to novel treatment CSCC strategies.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1

et al. 2019

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“…30 Huang B et al 31 observed that NEAT1 could promote pancreatic cancer progression through binding to miR-506-3p, a tumor suppressor reported in hepatocellular carcinoma. 32 Moreover, in the study of Yang H et al [33], they proved that the lncRNA, MIR31HG, was upregulated in PDAC through microarray gene-expression profile and qRT-PCR assay.…”

Section: Lncrnas and Micrornamentioning

confidence: 99%

The involvement of lncRNAs in the development and progression of pancreatic cancer

Qian

et al. 2017

Cancer Biology & Therapy

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Pancreatic cancer is one of the most malignant tumors that are difficult to diagnose at its early stage and there is no effective therapy. Recent studies uncovered that many non-protein-coding RNAs including the class of long noncoding RNAs (lncRNAs) are differentially expressed in various types of tumors and they are potent regulators of tumor progression and metastasis. LncRNA can mediate tumor initiation, proliferation, migration and metastasis through modulating epigenetic modification, alternative splicing, transcription, and protein translation. In this review, we discuss the molecular mechanism of lncRNAs in the involvement of tumor growth, survival, epithelial-mesenchymal transition, tumor microenvironment, cancer stem cells and chemoresistance in pancreatic ductal adenocarcinoma (PDAC).

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“…The therapies for HCC treatment have been notably promoted. Whereas, the overall rate of 5-year survival in HCC patients is only 12%, which remains dismal (2). Surgical resection, radiofrequency ablation and liver transplantation may benefit some patients with early-stage HCC.…”

Section: Introductionmentioning

confidence: 99%

miR-217 suppresses proliferation, migration, and invasion promoting apoptosis via targeting MTDH in hepatocellular carcinoma

Zhang

et al. 2017

Oncology Reports

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Hepatocellular carcinoma (HCC) has frequent incidence and the third highest mortality rate among cancers in the world. This study aimed to clarify the roles of miR-217 and metadherin (MTDH) in HCC. First, we identified that miR-217 expression was downregulated and MTDH expression was upregulated in the HCC tissues. Functional studies revealed that miR-217 negatively regulated MTDH expression via binding to the 3'-untranslated region of MTDH mRNA in the HCC cells. In our further studies, the miR-217 overexpression resulted in downregulation of MTDH expression in HCC cells. The miR-217 overexpression in HCC cells suppressed proliferation, migration, and invasion inducing apoptosis. Taken together, our study provides the initial evidence that the increase of MTDH expression is associated with the decrease of miR-217 expression in HCC. This study also suggests that miR-217 inhibits malignant progression of HCC in vitro and may be used for miRNA-based therapy, possibly via directly targeting MTDH.

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MiR-506 suppresses cell proliferation and tumor growth by targeting Rho-associated protein kinase 1 in hepatocellular carcinoma

Cited by 23 publications

References 19 publications

RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1

RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1

The involvement of lncRNAs in the development and progression of pancreatic cancer

miR-217 suppresses proliferation, migration, and invasion promoting apoptosis via targeting MTDH in hepatocellular carcinoma

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