miR-28-5p promotes the development and progression of ovarian cancer through inhibition of N4BP1

Xu, Juan; Jiang, Nan; Shi, Hongfu; Zhao, Shanshan; Yao, Shuzhong; Shen, Huimin

doi:10.3892/ijo.2017.3977

Cited by 24 publications

(43 citation statements)

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“…miRNAs participate in the modulation of greater than one-third of human genes (10). Studies have indicated that miRNAs are dysregulated in various types of human cancers, such as gastric cancer (11), hepatocellular carcinoma (12), bladder cancer (13), ovarian cancer (14) and breast cancer (15). Abnormally expressed miRNAs have been implicated in tumour initiation and progression, and may regulate a variety of important physiological events, including cell proliferation, cell cycle, apoptosis, angiogenesis, migration and invasion and metastasis (16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-197 inhibits gastric cancer progression by directly targeting metadherin

Liao

Zhou

et al. 2017

Mol Med Report

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Gastric cancer is the fifth most frequent malignancy and the fourth most common cause of cancer‑associated mortality worldwide. MicroRNAs (miRNAs) are a group of small RNAs that regulate several cellular processes. In particular, a large number of miRNAs are involved in gastric cancer formation and progression. Thus, miRNAs may be considered as effective diagnostic biomarkers and therapeutic methods for gastric cancer. The aim of the current study was to detect miRNA (miR)‑197 expression in gastric cancer and to investigate its biological role and associated mechanism in gastric cancer. In the present study, miR‑197 expression was demonstrated to be considerably downregulated in gastric cancer tissues and cell lines. Its low expression level was associated with tumour size, invasive depth, tumour‑node‑metastasis staging and lymph node metastasis. High expression of miR‑197 inhibited tumour cell proliferation and invasion in vitro. Subsequently, metadherin (MTDH) was identified as a direct target gene of miR‑197 in gastric cancer, and this was confirmed by bioinformatics analysis, Dual‑luciferase reporter assay, reverse transcription quantitative polymerase chain reaction and western blot analysis. MTDH expression was upregulated in gastric cancer and was inversely correlated with miR‑197 expression levels. In addition, MTDH overexpression prevented the proliferation and inhibited invasion induced by miR‑197 overexpression. In addition, miR‑197 was demonstrated to regulate the phosphatase and tensin homolog (PTEN)/AKT signalling pathway in gastric cancer. The results of the present study suggested that miR‑197 serves a tumour‑suppressing role in human gastric carcinogenesis and progression by regulating the MTDH/PTEN/AKT signalling pathway. The miR‑197/MTDH axis may provide a novel effective therapeutic target for patients with gastric cancer.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-197 inhibits gastric cancer progression by directly targeting metadherin

Liao

Zhou

et al. 2017

Mol Med Report

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“…For instance, it is a thrombopoietin receptor (TpoR, MPL) targeting miRNA, which is overexpressed in the platelets of patients with myeloproliferative neoplasms (MPNs) and its negative role in megakaryocyte differentiation leads to MPNs through the downregulation of MPL (59). In the process of ovarian cancer development and progression, miR-28-5p downregulates N4BP1, forces cancer cells to enter S phase, and promotes ovarian cancer cell proliferation and invasion (29). Taken together, miR-28-5p can function as either tumor suppressor genes or oncogenes, reflecting cell type-specific and tissue-specific roles of this miRNA.…”

Section: Discussionmentioning

confidence: 99%

“…We found 52 publications that related miR-28-5p with human tumors, with most of them serving as a tumor suppressor. Several important tumor-related genes were defined as the direct target for miR-28-5p, such as AKT in gastric cancer (8), N4BP1 in ovarian cancer (29), IL-34 (30) and IGF-1 (10) in hepatocellular carcinoma, and Rap1b in renal cell carcinoma (31). Among these, Rap1b has drawn our attention for the following reasons.…”

Section: Trpm7 Positively Regulated Rap1b Expression In Glioma Cellsmentioning

confidence: 99%

TRPM7 Induces Mechanistic Target of Rap1b Through the Downregulation of miR-28-5p in Glioma Proliferation and Invasion

et al. 2019

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Objectives: Our previous findings demonstrate that channel-kinase transient receptor potential (TRP) ion channel subfamily M, member 7 (TRPM7) is critical in regulating human glioma cell migration and invasion. Since microRNAs (miRNAs) participate in complex regulatory networks that may affect almost every cellular and molecular process during glioma formation and progression, we explored the role of miRNAs in human glioma progression by comparing miRNA expression profiles due to differentially expressed TRPM7. Methods: First, we performed miRNA microarray analysis to determine TRPM7's miRNA targets upon TRPM7 silencing in A172 cells and validated the miRNA microarray data using A172, U87MG, U373MG, and SNB19 cell lines by stem-loop RT-qPCRs. We next determined whether TRPM7 regulates glioma cell proliferation and migration/invasion through different functional domains by overexpressing wild-type human TRPM7 (wtTRPM7), two mutants with TRPM7's α-kinase domain deleted (kinase-DK), or a point mutation in the ATP binding site of the α-kinase domain (K1648R-KR). In addition, we determined the roles of miR-28-5p in glioma cell proliferation and invasion by overexpressing or under expressing miR-28-5p in vitro. Lastly, we determined whether a Ras-related small GTP-binding protein (Rap1b) is a target of miR-28-5p in glioma tumorigenesis. Results: The miRNA microarray data revealed a list of 16 downregulated and 10 upregulated miRNAs whose transcripts are significantly changed by TRPM7 knock-down. Cell invasion was significantly reduced in two TRPM7 mutants with inactive kinase domain, kinase, and K1648R transfected glioma cells. miR-28-5p overexpression suppressed glioma cells' proliferation and invasion, and miR-28-5p under expression led to a significant increase in glioma cell proliferation and migration/invasion compared to that of the controls. miR-28-5p suppressed glioma cell proliferation and migration by targeting Rap1b. Co-transfection of siRap1b with miR28-5p inhibitor reduced the glioma cell proliferation and invasion, caused by the latter. Wan et al. TRPM7 Induces Rap1b in Glioma Conclusions: These results indicate that TRPM7's channel activity is required for glioma cell growth while the kinase domain is required for cell migration/invasion. TRPM7 regulates miR-28-5p expression, which suppresses cell proliferation and invasion in glioma cells by targeting Rap1b signaling.

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Section: Introductionmentioning

confidence: 99%

“…miR-28-5p has been demonstrated to serve different roles in different cancer types (19,20). For instance, miR-28-5p promotes ovarian cancer progression through inhibition of NEDD4 binding protein 1 (20). In contrast, miR-28-5p is downregulated in colorectal cancer, and overexpression of miR-28-5p exhibits suppressive effects on colorectal cancer cell proliferation, migration and invasion in vitro, as well as tumor growth in vivo (19).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA‑UCA1 inhibits the proliferation and migration of melanoma cells through modulating the miR‑28‑5p/HOXB3 axis

et al. 2019

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Long non-coding RNA urothelial carcinoma-associated 1 (UCA1) functions as an oncogene in different human cancers, including melanoma. However, the molecular mechanism of UCA1 underlying melanoma progression still remains largely unknown. In the present study, reverse transcription quantitative polymerase chain reaction and western blot analyses were used to examine the mRNA and protein expression levels, respectively. Cell Counting Kit-8 and wound healing assays were conducted to study cell proliferation and migration, respectively. A luciferase reporter assay was used to confirm the targeting relationship. It was demonstrated that UCA1 expression was increased in melanoma tissues and cell lines. In addition, UCA1 expression was higher in melanoma tissues at stage III-IV than in tissues at stage I-II. Inhibition of UCA1 expression markedly reduced melanoma cell proliferation and migration. Further investigation revealed that UCA1 functioned in melanoma cells through directly binding with microRNA (miR)-28-5p. The expression of miR-28-5p was significantly reduced in melanoma tissues and had an inverse correlation with UCA1 expression. In addition, miR-28-5p expression was higher in melanoma tissues at advanced stages than in stage I-II tissues. Furthermore, homeobox (HOX)B3 was identified as a target gene of miR-28-5p in melanoma cells, and HOXB3 overexpression reversed the suppressive effects of UCA1 downregulation on melanoma cell proliferation and migration. Finally, HOXB3 was upregulated in melanoma tissues compared with its expression in adjacent tissues, and HOXB3 expression was increased in melanoma tissues at advanced stages. Taken together, the regulatory network of the UCA1/miR-28-5p/HOXB3 axis in melanoma was demonstrated for the first time in the present study, expanding the understanding of the molecular mechanism underlying melanoma progression. Future studies may further confirm the function of this signaling pathway in vivo.

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miR-28-5p promotes the development and progression of ovarian cancer through inhibition of N4BP1

Cited by 24 publications

References 0 publications

MicroRNA-197 inhibits gastric cancer progression by directly targeting metadherin

MicroRNA-197 inhibits gastric cancer progression by directly targeting metadherin

TRPM7 Induces Mechanistic Target of Rap1b Through the Downregulation of miR-28-5p in Glioma Proliferation and Invasion

Knockdown of lncRNA‑UCA1 inhibits the proliferation and migration of melanoma cells through modulating the miR‑28‑5p/HOXB3 axis

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