miR‐181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway

Wei, Zhonghua; Cui, Long; Mei, Zubing; Liu, Min; Zhang, Daoxiang

doi:10.1016/j.febslet.2014.03.037

Cited by 89 publications

(63 citation statements)

References 19 publications

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“…miR-181a mediates metabolic shift in colon cancer cells via the PTEN/ AKT pathway. 29 In this study, we found that miR-181a directly targeted 3′UTR of PTEN and luciferase report assay verified that PTEN is a target gene of miR-181a. The tumor suppressor PTEN is a phosphatase with sequence similarity to the cytoskeletal protein tensin.…”

Section: Discussionsupporting

confidence: 51%

Triptolide inhibits the growth of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and vitro

et al. 2017

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We aimed to study the anti-tumor effects of triptolide on osteosarcoma and the related molecular mechanisms. The cell viability, apoptosis portion, tumor size, tumor weight, and invasion of osteosarcoma cells were determined. The relative level of microRNA-181 in osteosarcoma tissues and the adjacent tissues was determined by quantitative realtime reverse transcription polymerase chain reaction. The target gene of microRNA-181a was determined and verified by luciferase report assay. At last, osteosarcoma cells were treated with triptolide and triptolide + microRNA-181a mimics to verify the relationship between triptolide and microRNA-181a. Triptolide inhibited the cell viability, promoted the apoptosis, decreased the tumor size and weight, and reduced the invasion of osteosarcoma cells. The level of microRNA-181a in osteosarcoma cells decreased significantly after treating with triptolide, and the relative level of microRNA-181a in osteosarcoma tissues was markedly higher than that in the adjacent tissues. PTEN was reported and verified the direct target gene of microRNA-181a. The overexpression of microRNA-181a decreased the inhibition of triptolide on osteosarcoma proliferation and promotion on osteosarcoma apoptosis. In conclusion, triptolide inhibited cell growth and invasion of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and vitro.

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Section: Discussionsupporting

confidence: 51%

Triptolide inhibits the growth of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and vitro

et al. 2017

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“…5a). Accumulating evidence has demonstrated that PTEN-Akt signaling pathway is tightly associated with the occurrence and development of a variety of tumors [31][32][33]; further investigation in the current study showed that WWP1 depletion increased PTEN level and reduced p-Akt level in MKN-45 and AGS cells but did not change total Akt level in MKN-45 and AGS cells (Fig. 5b-e).…”

Section: Wwp1 Downregulation Inactivated Pten-akt Signaling Pathwaysupporting

confidence: 52%

WWP1 as a potential tumor oncogene regulates PTEN-Akt signaling pathway in human gastric carcinoma

Zhang

et al. 2014

Tumor Biol.

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Whelming evidence has demonstrated that WW domain containing E3 ubiquitin protein ligase 1 (WWP1) participates in a wide variety of biological processes and is tightly related to the initiation and progression of many tumors. Currently, although mounting evidence supports a role of WWP1 in tumor promotion and tumorigenesis, the potential roles of WWP1 and its biological functions in gastric carcinoma are not fully understood. Here, we found that WWP1 messenger RNA (mRNA) and protein were highly expressed in gastric carcinoma tissues and cells. High WWP1 mRNA and protein levels were tightly related to differentiation status, TNM stage, invasive depth, lymph node metastasis, and poor prognosis in gastric carcinoma. Furthermore, WWP1 siRNA significantly decreased WWP1 protein level in MKN-45 and AGS cells; meanwhile, WWP1 depletion markedly inhibited tumor proliferation in vitro and in vivo, arrested cell cycle at G0/G1 phase, and induced cell apoptosis in MKN-45 and AGS cells. Most notably, WWP1 downregulation both inactivated PTEN-Akt signaling pathway in MKN-45 and AGS cells. Taken altogether, our findings suggest that WWP1 acts as an oncogenic factor and should be considered as a novel interfering molecular target for gastric carcinoma.

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“…Over the last decade, many miRNAs have been showed in regulating diverse biological events such as cell proliferation, differentiation and apoptotic processes [5][6][7], which are important in the development of cancer. Accumulated evidence indicated that aberrant expression of miRNAs associates with various types of cancer.…”

Section: Aimmentioning

confidence: 99%

MiRNA-20A Upregulates TAK1 and Increases Proliferation in Osteosarcoma Cells

Yuan

Zhao

et al. 2018

Future Oncol.

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Aim:The aim of this study is to explore the function of miR-20a in osteosarcoma. Materials & methods: miR-20a expression was measured by real-time PCR. miR-20a mimics, inhibitor and scramble siRNA were transfected into osteosarcoma cells to observe effects on colony formation and tumor growth. Moreover, relationships of miR-20a with TAK1 were investigated by western blot and luciferase activity. Results: We found that miR-20a was downregulated in osteosarcoma, and overexpression of miR-20a reduced colony formation and tumor growth. Furthermore, the data revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. Overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs. Conclusion: Our data identify the role of miR-20a in osteosarcoma growth, indicating its potential application in chemotherapy. Osteosarcoma is the most common primary malignant bone tumor with high morbidity in young adults and children, comprising 2.4% of all malignancies in pediatric patients and about 20% of all primary bone tumors [1]. It occurs mainly around regions with active bone growth and reparation. Osteosarcoma is highly aggressive and responded poorly to chemotherapy, and the 5-year survival rate for patients with metastatic osteosarcoma is only 14% [2]. Therefore, it is of extreme significance to elucidate novel molecular targets to develop alternative therapeutic target for this disease.miRNAs are a small family of noncoding RNAs that play important roles in the development of human diseases by negatively regulating gene expression at either post-transcriptional or translational levels [3,4]. Over the last decade, many miRNAs have been showed in regulating diverse biological events such as cell proliferation, differentiation and apoptotic processes [5][6][7], which are important in the development of cancer. Accumulated evidence indicated that aberrant expression of miRNAs associates with various types of cancer. These dysregulated miRNAs function as either oncogenes or tumor suppressors in carcinogenesis and progression of cancers [8,9]. Thus, to explore the aberrant miRNAs expression in osteosarcoma might lead to the discovery of novel miRNAs biomarkers.In this study, we found that miR-20a was downregulated in osteosarcoma samples and osteosarcoma cell lines, and the ectopic expression of miR-20a reduced cell colony formation in vitro and tumor growth in vivo. Furthermore, bioinformatic prediction and experimental validation revealed that the function of miR-20a was probably exerted via targeting the TAK1 expression. To translate these findings, overexpression of miR-20a sensitizes the osteosarcoma cells to chemotherapeutic drugs. Collectively, our data identify the key role of miR-20a in osteosarcoma growth, indicating its potential application in cancer chemotherapy.

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miR‐181a mediates metabolic shift in colon cancer cells via the PTEN/AKT pathway

Cited by 89 publications

References 19 publications

Triptolide inhibits the growth of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and vitro

Triptolide inhibits the growth of osteosarcoma by regulating microRNA-181a via targeting PTEN gene in vivo and vitro

WWP1 as a potential tumor oncogene regulates PTEN-Akt signaling pathway in human gastric carcinoma

MiRNA-20A Upregulates TAK1 and Increases Proliferation in Osteosarcoma Cells

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