MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

Zhou, Quan; Han, Leng; Zhou, Yang; Li, Yan

doi:10.1097/igc.0000000000000686

Cited by 61 publications

(59 citation statements)

References 29 publications

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“…Almeida et al reported that overexpression of miR-195 led to a decrease in osteogenic differentiation and proliferation rate in human primary mesenchymal stromal/stem cells (MSC) [55]. Zhou and colleagues reported that miR-195 suppressed cervical cancer migration and invasion through targeting Smad3 [56]. In the present study, we found that miR-195 was elevated in joint fluid specimens of patients with chronic cartilage lesions and in CH1M/CH3M chondrocytes.…”

Section: Discussionsupporting

confidence: 60%

Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway

Wang

Yang

Liu

et al. 2017

IJMS

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Slow growth and rapid loss of chondrogenic phenotypes are the major problems affecting chronic cartilage lesions. The role of microRNA-195 (miR-195) and its detailed working mechanism in the fore-mentioned process remains unknown. Fibroblastic growth factor 18 (FGF-18) plays a key role in cartilage homeostasis; whether miR-195 could regulate FGF-18 and its downstream signal pathway in chondrocyte proliferation and maintenance of chondrogenic phenotypes still remains unclear. The present research shows elevated miR-195 but depressed FGF-18 expressed in joint fluid specimens of 20 patients with chronic cartilage lesions and in CH1M and CH3M chondrocytes when compared with that in joint fluid specimens without cartilage lesions and in CH1W and CH2W chondrocytes, respectively. The following loss of function test revealed that downregulation of miR-195 by transfection of miR-195 inhibitors promoted chondrocyte proliferation and expression of a type II collagen α I chain (Col2a1)/aggrecan. Through the online informatics analysis we theoretically predicted that miR-195 could bind to a FGF-18 3′ untranslated region (3′UTR), also, we verified that a miR-195 could regulate the FGF-18 and its downstream pathway. The constructed dual luciferase assay further confirmed that FGF-18 was a direct target of miR-195. The executed anti-sense experiment displayed that miR-195 could regulate chondrocyte proliferation and Col2a1/aggrecan expression via the FGF-18 pathway. Finally, through an in vivo anterior cruciate ligament transection (ACLT) model, downregulation of miR-195 presented a significantly protective effect on chronic cartilage lesions. Evaluating all of the outcomes of the current research revealed that a decrease of miR-195 protected chronic cartilage lesions by promoting chondrocyte proliferation and maintenance of chondrogenic phenotypes via the targeting of the FGF-18 pathway and that the miR-195/FGF-18 axis could be a potential target in the treatment of cartilage lesions.

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Section: Discussionsupporting

confidence: 60%

Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway

Wang

Yang

Liu

et al. 2017

IJMS

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“…The function of miR-195 in CC has been widely probed, and it is certified that miR-195 inhibits CC cell proliferation, invasion and migration by targeting related genes, while the knockdown of miR-195 has the opposite impact on cell processes [3,6,24,25]. In this study, we further demonstrated that miR-195-5p could lessen CC cell proliferation and invasion ability via targeting MMP14.…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andsupporting

confidence: 49%

“…In previous studies, miR-195 has been found down-regulated significantly in CC tissues and cells [2,6]. For example, Zhang et al have reported miR-195 as a novel biomarker for detection of CC [5].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

“…Numerous researches have demonstrated that miRNA expression level is closely related to human cancer progression and metastasis. Previous studies have shown that various miRNAs are abnormally expressed in CC tissues, and miR-195 is one of them [3,6]. Some studies have been done to elucidate the role of miR-195 in CC cells, and it is believed that miR-195 functions as a tumor suppressing miRNA in CC [2].…”

Section: Introductionmentioning

confidence: 99%

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The Effects of miR-195-5p/MMP14 on Proliferation and Invasion of Cervical Carcinoma Cells Through TNF Signaling Pathway Based on Bioinformatics Analysis of Microarray Profiling

Ren

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study is aimed at identification of miR-195-5p/MMP14 expression in cervical cancer (CC) and their roles on cell proliferation and invasion profile of CC cells through TNF signaling pathway in CC. Methods: Microarray analysis, gene set enrichment analysis (GSEA) and DAVID were used to analyze differentially expressed miRNAs, mRNAs and signaling pathways. MiR-195-5p and MMP14 expression levels in CC cell were determined by qRT-PCR. Western blot was employed to measure MMP14 and TNF signaling pathway-relating protein level. Luciferase reporter system was used to confirm the targeting relationship between MMP14 and miR-195-5p. Cell proliferation and invasion was respectively deeded by CCK8, transwell. In vivo experiment was carried out to study the impact of MMP14 and miR-195-5p on CC development in mice. Results: The microarray analysis and the results of qRT-PCR determined that miR-195-5p was under-expressed and MMP14 was over-expressed in CC cells. GSEA and DAVID analysis showed that TNF signaling pathway was regulated by miR-195-5p/MMP14 and activated in cervical carcinoma cells. The miR-195-5p and MMP14 have a negative regulation relation. In vivo experiment found that down-regulated MMP14 and up-regulated miR-195-5p suppressed the tumor development. Conclusion: Our results suggest that MMP14 is a direct target of miR-195-5p, and down-regulated MMP14 and up-regulated miR-195-5p suppressed proliferation and invasion of CC cells by inhibiting TNF signaling pathway.

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“…Furthermore, miR-16-2-3p has been shown up-regulated in serum pointing out the role of miR-16 in cervical carcinogenesis [40]. On the other hand, miR-195 is shown down-regulated in cervical cancer and its overexpression inhibits proliferation, G1-S transition, migration and invasion through Cyclin D1, Cyclin D2, MYB proto-oncogene, transcription factor (MYB) and Smad 3 down-regulation via 3′UTR [44,45,46,47]. …”

Section: Oncogenic Mir-15 Family Participates In Cervical Cancermentioning

confidence: 99%

Use of Mature miRNA Strand Selection in miRNAs Families in Cervical Cancer Development

Granados-López

Ruiz-Carrillo

Servín-González

et al. 2017

IJMS

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Aberrant miRNA expression is well recognized as a cancer hallmark, nevertheless miRNA function and expression does not always correlate in patients tissues and cell lines studies. In addition to this issue, miRNA strand usage conduces to increased cell signaling pathways modulation diversifying cellular processes regulation. In cervical cancer, 20 miRNA families are involved in carcinogenesis induction and development to this moment. These families have 5p and 3p strands with different nucleotide (nt) chain sizes. In general, mature 5p strands are larger: two miRNAs of 24 nt, 24 miRNAs of 23 nt, 35 miRNAs of 22 nt and three miRNAs of 21 nt. On the other hand, the 3p strands lengths observed are: seven miRNAs of 23 nt, 50 miRNAs of 22 nt, six miRNAs of 21 nt and four miRNAs of 20 nt. Based on the analysis of the 20 miRNA families associated with cervical cancer, 67 3p strands and 65 5p strands are selected suggesting selectivity and specificity mechanisms regulating cell processes like proliferation, apoptosis, migration, invasion, metabolism and Warburg effect. The insight reviewed here could be used in the miRNA based therapy, diagnosis and prognosis approaches.

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MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

Abstract: The newly identified miR-195/Smad3 pathway provides an insight into cervical cancer metastasis and may represent a novel therapeutic target.

Cited by 61 publications

References 29 publications

Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway

Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway

The Effects of miR-195-5p/MMP14 on Proliferation and Invasion of Cervical Carcinoma Cells Through TNF Signaling Pathway Based on Bioinformatics Analysis of Microarray Profiling

Use of Mature miRNA Strand Selection in miRNAs Families in Cervical Cancer Development

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