miR-125a inhibits the migration and invasion of liver cancer cells via suppression of the PI3K/AKT/mTOR signaling pathway

Tang, Hao; Li, Rong‐Ping; Liang, Ping; Zhou, Ya‐Long; Wang, Guang‐Wei

doi:10.3892/ol.2015.3264

Cited by 78 publications

(65 citation statements)

References 30 publications

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“…MicroRNA‐125a‐5p has been demonstrated as an independent prognostic factor in gastric cancer and inhibiting the gastric cancer development,20 through targeting oncogenes such as vascular endothelial growth factor A21 and E2F transcription factor 3 22. Overexpressing miR‐125a‐5p could inhibit the cancer proliferation and migration 23, 24…”

Section: Introductionmentioning

confidence: 99%

Retracted: Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

Cai

Chen

Shen

et al. 2018

J Cellular Molecular Medi

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Emerging evidence suggests that microRNAs (miRNAs) serve an important role in tumorigenesis and development. Although the low expression of miR‐125a‐5p in gastric cancer has been reported, the underlying mechanism remains unknown. In the current study, the low expression of miR‐125a‐5p in gastric cancer was verified in paired cancer tissues and adjacent non‐tumour tissues. Furthermore, the GC islands in the miR‐125a‐5p region were hypermethylated in the tumour tissues. And the hypermethylation was negatively correlated with the miR‐125a‐5p expression. Target gene screening showed that the histone methyltransferase Suv39H1 was one of the potential target genes. In vitro studies showed that miR‐125a‐5p could directly suppress the Suv39H1 expression and decrease the H3K9me3 levels. On the other hand, the Suv39H1 could induce demethylation of miR‐125a‐5p, resulting in re‐activation of miR‐125a‐5p. What is more, overexpessing miR‐125a‐5p could also self‐activate the silenced miR‐125a‐5p in gastric cancer cells, which suppressed cell migration, invasion and proliferation in vitro and inhibited cancer progression in vivo. Thus, we uncovered here that the epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer, suggesting that miR‐125a‐5p might be not only the potential prognostic value as a tumour biomarker but also potential therapeutic targets in gastric cancer.

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Section: Introductionmentioning

confidence: 99%

Retracted: Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

Cai

Chen

Shen

et al. 2018

J Cellular Molecular Medi

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“…The increased methylation of miR-125a promoter may lead to a decrease in transcription factor recruitment to the promoter, thus resulting in a decrease in the expression of miR-125a. Previous studies have shown that miR-125a plays a role as a tumor suppressor genes in prostate cancer [15], glioblastoma [16, 17], breast cancer [18], liver cancer [7, 19], gastric cancer [11, 20] and cervical cancer [21, 22]. Wang et al found that EGFR inhibited the invasion of lung cancer cells by activating miR-125a, and miR-125a could also inhibit the proliferation of vascular endothelial cells [23].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Tao

Shen

Luo

et al. 2017

Cell Physiol Biochem

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Background/Aims: Increasing evidence has shown that miR-125a plays important role in human cancer progression. However, little is known about the function of miR-125a in osteosarcoma. Methods: The expression of miR-125a in osteosarcoma tissues and cell lines were examined by qRT-PCR. The biological role of miR-125a in osteosarcoma cell proliferation was examined in vitro. The targets of miR-125a were identified by a dual-luciferase reporter assay. Results: The results showed that the expression of miR-125a expression is significantly lower in osteosarcoma tissues and cell lines. Survival curves showed that the survival of patients in high miR-125a expression was significantly longer than that of patients with low miR-125a expression, and multivariate analysis suggested that miR-125a is an independent prognostic factor for osteosarcoma patients. In addition, it was found in this study that miR-125a can inhibit the growth of osteosarcoma cells. The dual-luciferase reporter assay demonstrated that E2F2 is a novel target gene for miR-125a. In addition, in a recovery experiment, it was shown that miR-125a inhibits the biological function of osteosarcoma cells by inhibiting the expression of E2F2. Conclusion: Our results suggest that miR-125a acts as a tumor suppressor via regulation of E2F2 expression in osteosarcoma progression, and miR-125a may represent a novel therapeutic target for the treatment of osteosarcoma.

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“…Moreover, microRNAs can regulate the PI3K/Akt/mTOR pathway in HCC. Tang et al[114] reported that miR-125a suppress HCC progression by inhibiting the PI3K/Akt pathway. Fang et al[115] investigated the molecular mechanism of miR-7 in HCC growth and metastasis and revealed the regulatory role of miR-1 in the PI3K/Akt pathway via targeting PIK3CD, mTOR and p70S6K.…”

Section: Regulatory Mechanism Of Glucose Metabolic Reprogrammingmentioning

confidence: 99%

Reprogramming of glucose metabolism in hepatocellular carcinoma: Progress and prospects

Shang

Wang

2016

WJG

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Hepatocellular carcinoma (HCC) is one of the most lethal cancers, and its rate of incidence is rising annually. Despite the progress in diagnosis and treatment, the overall prognoses of HCC patients remain dismal due to the difficulties in early diagnosis and the high level of tumor invasion, metastasis and recurrence. It is urgent to explore the underlying mechanism of HCC carcinogenesis and progression to find out the specific biomarkers for HCC early diagnosis and the promising target for HCC chemotherapy. Recently, the reprogramming of cancer metabolism has been identified as a hallmark of cancer. The shift from the oxidative phosphorylation metabolic pathway to the glycolysis pathway in HCC meets the demands of rapid cell proliferation and offers a favorable microenvironment for tumor progression. Such metabolic reprogramming could be considered as a critical link between the different HCC genotypes and phenotypes. The regulation of metabolic reprogramming in cancer is complex and may occur via genetic mutations and epigenetic modulations including oncogenes, tumor suppressor genes, signaling pathways, noncoding RNAs, and glycolytic enzymes etc. Understanding the regulatory mechanisms of glycolysis in HCC may enrich our knowledge of hepatocellular carcinogenesis and provide important foundations in the search for novel diagnostic biomarkers and promising therapeutic targets for HCC.

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miR-125a inhibits the migration and invasion of liver cancer cells via suppression of the PI3K/AKT/mTOR signaling pathway

Cited by 78 publications

References 30 publications

Retracted: Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

Retracted: Epigenetic silenced miR‐125a‐5p could be self‐activated through targeting Suv39H1 in gastric cancer

MicroRNA-125a Regulates Cell Proliferation Via Directly Targeting E2F2 in Osteosarcoma

Reprogramming of glucose metabolism in hepatocellular carcinoma: Progress and prospects

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