miR‐342‐3p suppresses proliferation, migration and invasion by targeting FOXM1 in human cervical cancer

Li, Xu-ri; Chu, Huijun; Lv, Teng; Wang, Lei; Kong, Shoufang; Dai, Sheng

doi:10.1016/j.febslet.2014.07.020

Cited by 102 publications

(90 citation statements)

References 25 publications

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“…For instance, Zhou et al (26) demonstrated that that miR-107 directly targeted myeloid cell leukemia-1 and activated the ATR serine/threonine kinase/checkpoint kinase 1 pathway to inhibit the proliferation, migration and invasiveness of cervical cancer cells. Li et al (27) reported that the overexpression of miR-342-3p inhibits cell proliferation, migration and invasion in cervical cell lines by targeting mammalian transcription factor forkhead box M1. Wen et al (28) reported that miR-506 induced cell cycle arrest at the G1/S transition, enhanced the apoptosis and chemosensitivity of cervical cancer cells, and inhibited cervical cancer growth in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-138 inhibits proliferation, migration and invasion through targeting hTERT in cervical cancer

et al. 2016

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Abstract.A growing body of evidence suggests that microRNA-138 (miR-138) functions as a tumor suppressor, and is involved in tumor initiation, development and metastasis in certain types of human cancers. However, the function and underlying molecular mechanism of miR-138 in cervical cancer remains unclear. Therefore, the purpose of the present study was to investigate the clinical significance of miR-138 expression in cervical cancer, and to evaluate its role and underlying mechanisms in cervical cancer. The present study indicated that miR-138 expression was significantly downregulated in cervical cancer tissues and cell lines, and that the low miR-138 expression was negatively associated with advanced FIGO stage and lymph node metastasis (P<0.01). Functional analyses indicated that the overexpression of miR-138 in cervical cancer cells inhibited cell proliferation, migration and invasion, induced cell apoptosis in vitro, and suppressed tumor growth in a nude mice model. Luciferase reporter assays confirmed that human telomerase reverse transcriptase was a novel target gene of miR-138. The findings of the present study suggested that miR-138 could be a potential candidate for cervical cancer therapeutics.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-138 inhibits proliferation, migration and invasion through targeting hTERT in cervical cancer

et al. 2016

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“…A high level of miR-342-3p has been associated with significantly worse survival in patients with colon cancer [50]. More recently, it has been reported that miR-342-3p suppresses proliferation, migration and invasion by targeting FOXM1 in human cervical cancer [51]. This miR has also been found to be significantly elevated in irritable bowel syndrome patients [52].…”

Section: Discussionmentioning

confidence: 99%

Obesity-Associated MiR-342-3p Promotes Adipogenesis of Mesenchymal Stem Cells by Suppressing CtBP2 and Releasing C/EBPα from CtBP2 Binding

Wang

et al. 2015

Cell Physiol Biochem

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Background/Aims: The elucidation of the molecular mechanism of adipocyte differentiation in mesenchymal stem cells is of essential importance for the development of treatments for metabolic diseases, such as obesity and diabetes. Methods: The expression levels of miR-342-3p and carboxy-terminal binding protein 2 (CtBP2) were regulated by oligonucleotide transfection. Adipogenic differentiation was induced by adipogenic medium containing indomethacin, dexamethasone and 3-isobutyl-1-methylxanthine on day 12, as determined by Oil Red O staining and triglyceride concentration assay to assess intracellular lipid accumulation. The induction of adipocyte-specific transcription factors and markers was detected by qRT-PCR and western blot. The regulation of CtBP2 expression by miR-342-3p was determined by western blot, qRT-PCR, luciferase reporter assay, ChIP assay and functional experiments. Results: We revealed that miR-342-3p was enriched in the adipose tissue of obese mice, and its expression was significantly elevated during adipogenic differentiation in both human mesenchymal stem cells (hMSCs) and 3T3L1 cells. Using gain- and loss-of-function assays, we demonstrated that the overexpression of miR-342-3p markedly promoted the differentiation of hMSCs into an adipogenic lineage. Adipogenesis was significantly blocked by miR-342-3p downregulation. We identified and validated that CtBP2 was a direct target of miR-342-3p in this process. The effects of the inhibition of CtBP2 were similar to those of miR-342-5p overexpression on adipogenic differentiation, promoting the release of C/EBPα from CtBP2 binding. Conclusion: miR-342-3p is a powerful enhancer of the adipogenesis of human adipose-derived MSCs that acts by inhibiting CtBP2 and releasing the key adipogenic regulator C/EBPα from CtBP2 binding, subsequently activating the expression of adipogenic transcription factors and markers.

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“…Previous studies have indicated that, during the embryonic period, FOXM1 is overexpressed in all tissues (15); however, in adulthood, FOXM1 expression only occurs in the tissues with active proliferation and metabolism (16). In various types of tumor cells, FOXM1 is highly expressed in the nucleus and cytoplasm, and causes the dysfunction of regulation processes (17)(18)(19)(20)(21). In particular, FOXM1 controls mitotic entry by the periodic upregulation of a group of genes that are maximally expressed as cells progress through the late G2 and into the M phase (14).…”

Section: Introductionmentioning

confidence: 99%

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

Zhang

Kong

2016

Oncology Letters

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Abstract. The regulation of entry into and progression through mitosis is important for cell proliferation. Polo-like kinase 1 (PLK1) is involved in multiple stages of mitosis. Forkhead box protein M1 (FOXM1) has multiple functions in tumorigenesis and, in elevated levels, is frequently associated with cancer progression. The present study reports that FOXM1, a substrate of PLK1, controls the transcription mechanism that mediates the PLK1-dependent regulation of the cell cycle. The present study investigated the expression of PLK1 and FOXM1 in the clear renal cell carcinoma 769-P and ACHN cell lines, and indicated that the expression of PLK1 and FOXM1 are correlated in human renal cell cancer cell lines and that the suppression of PLK1 may decrease the expression of FOXM1. The knockdown of FOXM1 or PLK1 in renal cell cancer cell lines caused cell cycle progression to be blocked. As a result, the present study indicated the involvement of FOXM1 in PLK1-regulated cell cycle progression.

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miR‐342‐3p suppresses proliferation, migration and invasion by targeting FOXM1 in human cervical cancer

Cited by 102 publications

References 25 publications

MicroRNA-138 inhibits proliferation, migration and invasion through targeting hTERT in cervical cancer

MicroRNA-138 inhibits proliferation, migration and invasion through targeting hTERT in cervical cancer

Obesity-Associated MiR-342-3p Promotes Adipogenesis of Mesenchymal Stem Cells by Suppressing CtBP2 and Releasing C/EBPα from CtBP2 Binding

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

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