miR-506 suppresses cervical cancer cell proliferation both in vitro and in vivo

Gong, Ming; Chen, C; Zhao, Huihui; Sun, Mei; Song, Mengxiong

doi:10.4149/neo_2018_170112n25

Cited by 16 publications

(10 citation statements)

References 33 publications

(45 reference statements)

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“…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. Further analyzes revealed the potential use of miR-506 in suppressing the proliferation of cervical cancer cells [9]. In gastric cancer, miR-506 was found to suppress metastatic invasion and angiogenesis by targeting ETS1 [10].…”

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RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1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RETRACTED ARTICLE: miR-506 contributes to malignancy of cutaneous squamous cell carcinoma via targeting of P65 and LAMC1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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“…[22][23][24] For instance, Gong et al proved that miR-506 inhibited cervical cancer cell proliferation both in vitro and in vivo. [22][23][24] For instance, Gong et al proved that miR-506 inhibited cervical cancer cell proliferation both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…miR-506 has been reported to play a suppressive role in several human tumors including gastric cancer, cervical cancer, and colorectal cancer. [22][23][24] For instance, Gong et al proved that miR-506 inhibited cervical cancer cell proliferation both in vitro and in vivo. Besides, Lei et al 25 reported that miR-506 regulated cell proliferation via downregulating iASPP expression in ovarian cancer.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

Yan

Silva

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) have been reported to be abnormally expressed in several cancers and associated with the proliferation of cancer cells. The objective of this study was to investigate the role and the underlying mechanisms of DQ786243 in ovarian cancer. In the current study, DQ786243 was specifically upregulated in ovarian cancer tissues and cell lines. Knockdown of DQ786243 inhibited the ability of cell migration, invasion, proliferation, colony formation and wound healing, whereas promoted cell apoptosis and induced G0/G1 cell cycle arresting. By using online tools and mechanistic analysis, we demonstrated that DQ786243 could directly bind to microRNA-506 (miR-506) and downregulate its expression. Moreover, DQ786243 reversed the inhibitory effect of miR-506 on the growth of ovarian cancer cells, which might be involved in the derepression of cAMP responsive element binding protein 1 (CREB1) expression. Further investigation into the mechanisms showed that knockdown of DQ786243 inhibited the epithelial to mesenchymal transition (EMT) process in ovarian cancer cells. Finally, xenograft experiments further confirmed that knockdown of DQ786243 notably suppressed the proliferation and EMT process in vivo. Taken together, our study showed for the first time that DQ786243 interacted with miR-506 and promoted progression of ovarian cancer via targeting CREB1 in ovarian cancer. The results might help to probe the feasibility of lncRNA-directed therapy for this deadly disease.

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“…The impact of RSC on RANKL-induced osteoclastogenesis was examined by He and colleagues 17 . Additional assessment demonstrated the possible application of miR-506 in repressing the proliferation of cervical cancer cells 22 . The transition from epithelium to mesenchymal cells was modulated by miR-506 in breast cancer cells 21 .…”

Section: Introductionmentioning

confidence: 99%

“…Remarkable miR-506 downregulation was revealed in cervical cancer cell samples (C33A and HeLa) compared with that of control cells and the surrounding normal tissues. Additional assessment demonstrated the possible application of miR-506 in repressing the proliferation of cervical cancer cells 22 . It was discovered that miR-506 repressed metastatic invasion as well as vessel generation by targeting ETS1 in gastric cancer 23…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐506 upregulation contributes to sirtuin 1 inhibition of osteoclastogenesis in bone marrow stromal cells induced by TNF‐α treatment

Shu

Miao

et al. 2019

Cell Biochemistry & Function

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As a deacetylase relying on NAD, sirtuin 1 (SIRT1) has been proven to inhibit osteoclastogenesis directly by repressing reactive oxygen species (ROS) production and TRPV1 channel stimulation modulated by TNF-α. MicroRNAs do not have coding functions, but they influence the expression of particular genes after transcription.Nevertheless, the current understanding of the impact of SIRT1 on osteoclastogenesis is insufficient. Our research explored whether and how miRNAs contributed to osteoclast differentiation modulated by SIRT1 in vitro. In osteoclastogenesis induced by RANKL in bone marrow-derived macrophages (BMMs), repression of SIRT1 expression and enhancement of miR-506 expression were discovered. Transfection with an miR-506 inhibitor repressed miR-506 concentration in BMMs treated with RANKL. Additional research revealed that BMMs with repressed miR-506 treated with RANKL displayed phenotypes with suppressed osteoclastogenesis, as demonstrated by TRAP staining, reduced function, decreased expression of osteoclast markers and correlated genes, and reduced multinuclear cell quantity. Bioinformatics prediction outcomes and the dual-luciferase reporter test suggested that miR-506 targeted the SIRT1 3′-UTR for silencing. Decreased miR-506 in BMMs induced by RANKL caused SIRT1 upregulation. Additionally, treatment with EX-527 (SIRT1 repressor) or SIRT1 silencing attenuated repression caused by miR-506 depletion in BMMs treated with RANKL. Furthermore, TNF-α was repressed via miR-506 inhibition but was enhanced following EX-527 incubation as well as SIRT1 depletion.TRPV1 channel stimulation and ROS generation, which was related to osteoclastogenesis, were reduced via miR-506 depletion. miR-506 modulated osteoclastogenesis by targeting SIRT1 expression in part through modulation of the TRPV1 channel, ROS production, and TNF-α. KEYWORDSbone marrow-derived macrophages, miR-506, osteoclastogenesis, reactive oxygen species, sirtuin 1, TNF-α, transient receptor potential vanilloid 1 Shu Yan and Lujie Miao contributed equally to this work and should be considered as equal first coauthors.

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miR-506 suppresses cervical cancer cell proliferation both in vitro and in vivo

Cited by 16 publications

References 33 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

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

MicroRNA‐506 upregulation contributes to sirtuin 1 inhibition of osteoclastogenesis in bone marrow stromal cells induced by TNF‐α treatment

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