MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer

Qw, Li; Zhou, Tian; F, Wang; Jiang, Mingrui; Cb, Liu; Kr, Zhang; Zhou, Qing; Tian, Zhongxian; Kw, Hu

doi:10.4238/2015.december.8.2

Cited by 17 publications

(14 citation statements)

References 33 publications

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“…Several targets of miR-215 have been identified, including runt-related transcription factor 1 (28) and RB transcriptional corepressor 1 (26) in gastric cancer, X-linked inhibitor of apoptosis in epithelial ovarian cancer (30), and zinc finger E-box binding homeobox 2 in pancreatic cancer (31) and non-small cell lung cancer (32). In our study, AKT1 was validated as a novel target of miR-215 through four experiments.…”

Section: Discussionmentioning

confidence: 74%

“…However, previous studies have also demonstrated that miR-215 may be downregulated in epithelial ovarian (30), pancreatic (31), non-small cell lung (32), breast (33) and colon (34) cancer. In the study on pancreatic cancer, a low expression level of miR-215 was significantly associated with a large tumor size, an advanced TNM stage, a high extent of lymph node metastasis and vessel invasion, and lower overall survival time; multivariate regression analysis demonstrated that miR-215 underexpression was an independent unfavorable prognostic factor for patients (31). miR-215 expression was also reported to be associated with a higher tumor grade, human epidermal growth factor receptor 2 (HER2)-positivity, HER2-positive breast cancer subtype and lymph node metastasis in breast cancer (33).…”

Section: Discussionmentioning

confidence: 96%

“…The expression level of miR-215 was demonstrated to be associated with the International Federation of Gynecology and Obstetrics stage, the histological grade, and the extents of vascular invasion and lymph node metastasis of cervical cancer; the 5-year survival rate was lower in patients with stage II cervical cancer who exhibited miR-215 overexpression (29). However, previous studies have also demonstrated that miR-215 may be downregulated in epithelial ovarian (30), pancreatic (31), non-small cell lung (32), breast (33) and colon (34) cancer. In the study on pancreatic cancer, a low expression level of miR-215 was significantly associated with a large tumor size, an advanced TNM stage, a high extent of lymph node metastasis and vessel invasion, and lower overall survival time; multivariate regression analysis demonstrated that miR-215 underexpression was an independent unfavorable prognostic factor for patients (31).…”

Section: Discussionmentioning

confidence: 97%

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MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1

et al. 2017

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Abstract. There are accumulating reports that microRNAs are dysregulated in a number of human cancer types, and that they may function as tumor suppressors or oncogenes in tumorigenesis and tumor development. microRNA-215 (miR-215) has been identified as a tumor suppressor in epithelial ovarian, pancreatic, non-small cell lung and colon cancer, whereas it may act as an oncogene in gastric and cervical cancer. The role of miR-215 in breast cancer carcinogenesis and progression has yet to be elucidated. In the present study, the expression level of miR-215 was determined in breast cancer tissues and cell lines using the reverse transcription-quantitative polymerase chain reaction. The effects of miR-215 overexpression on proliferation and the invasive capacity of breast cancer cells were assessed using MTT and cell invasion assays. The results revealed that miR-215 was significantly downregulated in breast cancer tissues and cell lines. Restoration of miR-215 expression inhibited the proliferation and invasion of breast cancer cells. The underlying molecular mechanism for the suppression of proliferation and invasion by miR-215 was investigated. AKT serine/threonine kinase 1 (AKT1) was validated as a novel direct target of miR-215, and the effect of AKT1 small interfering RNA mimicked the effect of miR-215 overexpression in breast cancer cells. These results indicated that miR-215 acted as a tumor suppressor, and that its downregulation in tumor tissues may contribute to the carcinogenesis and progression of breast cancer, indicating that miR-215 may be a novel therapeutic target for the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

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MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1

et al. 2017

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“…miR‐215 is decreased in various cancers . miR‐215 can repress breast cancer progression by targeting AKT .…”

Section: Discussionmentioning

confidence: 99%

“…miR-215 is decreased in various cancers. [28][29][30] miR-215 can repress breast cancer progression by targeting AKT. 31 miR-215 can inhibit epithelial ovarian cancer progression via regulating NOB1.…”

Section: Discussionmentioning

confidence: 99%

Insight into the molecular mechanism of LINC00152/miR‐215/CDK13 axis in hepatocellular carcinoma progression

Wang

Zhang

et al. 2019

J of Cellular Biochemistry

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Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world. Nevertheless, its underlying molecular mechanisms are largely unknown. LINC00152 are recently investigated in several cancer types. In our current investigation, we observed LINC00152 was obviously upregulated in HCC cells. LINC00152 was significantly downregulated by infecting LV‐shLINC00152 in HepG2 and SNU449 cells. Loss of LINC00152 remarkably repressed HCC cell proliferation, cell colony formation, induced cell apoptosis, and restrained cell migration/invasion. Growing evidence has reported long noncoding RNAs can sponge microRNAs to modulate cancer process. Here, we indicated miR‐215 was greatly decreased in HCC and LINC00152 regulated HCC development via sponging miR‐215. For another, the binding association between LINC00152 and miR‐215 was proved by a series of functional assays. CDK13 was predicted as the target of miR‐215. Upregulation of miR‐215 greatly depressed CDK13 in HCC cells. Subsequently, the in vivo results demonstrated that silence of LINC00152 restrained HCC development via modulating miR‐215 to up‐regulate CDK13. Therefore, it was revealed that LINC00152 contributed to the progression of HCC by the modulation of miR‐215 and CDK13.

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miR‐215‐5p decreases migration and invasion of trophoblast cells through regulating CDC6 in preeclampsia

Yang

Meng

2020

Cell Biochemistry & Function

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Preeclampsia (PE) is a serious disease that occurs after 20 weeks during pregnancy.There are some aberrant microRNAs (miRNAs) that are associated with the etiology of PE. As discovered by scholars, there was an increased level of miR-215-5p in plasma of PE patients compared with the control group; nonetheless, there is still no knowledge of the mechanism of miR-215-5p in PE. We carried out the comparison of the expression levels of miR-215-5p, and the supposed target gene cell division cycle 6 (CDC6) in 30 placentas from PE patients as well as 30 placentas from normal pregnant women. The verification of the impacts of miR-215-5p and CDC6 was carried out by functional assays in HTR-8/SVneo cells transfected with the miR-215-5p mimic or siR-CDC6. As indicated by findings, miR-215-5p showed an apparent increase; conversely, CDC6 was inhibited in the experiment group. The upregulation of miR-215-5p inhibited both the migration and invasive potential of trophoblasts, besides decreasing the G1-S transition and downregulating CDC6 in HTR-8/SVneo cells; nonetheless, it did not significantly impact the cell proliferation. Furthermore, siR-CDC6 replicated the functions of the miR-215-5p mimic. Also, the miR-215-5p mimic and siR-CDC6 both decreased the epithelial-mesenchymal transition (EMT) with additional E-cadherin level and decreased the expressions of N-cadherin as well as vimentin in trophoblast cells. To conclude, miR-215-5p decreased not only the migration but also the invasion of trophoblasts through regulating CDC6, which indicated that miR-215-5p might be associated with the etiology of PE.Significance of the study: More and more attention has been paid on the roles of miRNAs in the pathogenesis of PE. However, there is no study of miR-215-5p in the etiology of PE. We first investigated the mechanism of miR-215-5p in placental tissues and HTR-8/SVneo cells. It was suggested that miR-215-5p decreased the abilities of migration and invasion of trophoblasts through regulating CDC6 in PE. miR-215-5p might be used as an target for the early diagnosis and treatment of PE in the future. K E Y W O R D S preeclampsia, miR-215-5p, CDC6, EMT, placenta Abbreviations: CCK-8, Cell Counting Kit-8; CDC6, cell division cycle 6; cDNA, complementary DNA; DMEM, Dulbecco's modified Eagle's medium; EMT, epithelial-mesenchymal transition.; FBS, fetal bovine serum; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; miRNA, microRNA; PBS, phosphate-buffered saline solution; PE, preeclampsia; PI, propidium iodide; PVDF, polyvinylidene fluoride; SDS-PAGE, sodium dodecyl sulfate polyacrylamide gel electrophoresis.

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MicroRNA-215 functions as a tumor suppressor and directly targets ZEB2 in human pancreatic cancer

Cited by 17 publications

References 33 publications

MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1

MicroRNA-215 acts as a tumor suppressor in breast cancer by targeting AKT serine/threonine kinase 1

Insight into the molecular mechanism of LINC00152/miR‐215/CDK13 axis in hepatocellular carcinoma progression

miR‐215‐5p decreases migration and invasion of trophoblast cells through regulating CDC6 in preeclampsia

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