MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

Ren, Ping; Gong, Fangchao; Zhang, Yan; Jiang, Jindong; Zhang, Hong

doi:10.1007/s13277-015-4150-3

Cited by 70 publications

(57 citation statements)

References 44 publications

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“…miR-92a-3p was evaluated as a diagnostic biomarker in CRC in previous study [14, 38, 39]. As a member of large cluster miR-17-92, miR-92a-3p has an important role as an oncogene in some cancers [40, 41]. Upregulation of the miR-92a-3p has been shown to disrupt the functions of several important factors of growth and division in colorectal cells [42].…”

Section: Discussionmentioning

confidence: 99%

A panel of microRNA signature in serum for colorectal cancer diagnosis

et al. 2017

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Dysregulated expression of specific microRNAs (miRNAs) in serum has been recognised as promising diagnostic biomarkers for colorectal cancer (CRC). In the initial screening phase, a total of 32 differentially expressed miRNAs were selected by quantitative reverse transcription polymerase chain reaction (qRT-PCR) based Exiqon panel with 3 CRC pool samples and 1 normal control (NC) pool. Using qRT-PCR, selected serum miRNAs were further confirmed in training (30 CRC VS. 30 NCs) and testing stages (136 CRC VS. 90 NCs). We identified that serum levels of miR-19a-3p, miR-21-5p and miR-425-5p were significantly higher in patients with CRC than in NCs. The areas under the receiver operating characteristic (ROC) curve of the three-miRNA panel were 0.86, 0.74 and 0.87 for the training, testing and the external validation stages (30 CRC VS. 18 NCs), respectively. Significantly, elevated expression of the three miRNAs was also observed in CRC tissues (n = 24). Furthermore, the expression levels of the three miRNAs were significantly elevated in exosomes from CRC serum samples (n = 10). In conclusion, we identified a serum three-miRNA panel for the diagnosis of CRC.

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Section: Discussionmentioning

confidence: 99%

A panel of microRNA signature in serum for colorectal cancer diagnosis

et al. 2017

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“…In recent studies, it was observed that overexpression of miR-92a-3p can disrupt PI3K/Akt/mTOR pathway by targeting two negative regulatory factors of this pathway, PTEN and PHLPP [29, 31]. Different studies have reported that overexpression of miR-92a-3p is involved in the development of metastasis and correlates with survival in different malignancies [32–34].…”

Section: Discussionmentioning

confidence: 99%

Urinary cell microRNA-based prognostic classifier for non-muscle invasive bladder cancer

et al. 2017

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Current prognostic tools for non-muscle invasive bladder cancer (NMIBC) do not have enough discriminative capacity to predict the risk of tumour progression. This study aimed to identify urinary cell microRNAs that may be useful as non-invasive predictive biomarkers of tumour progression in NMIBC patients. To this end, 210 urine samples from NMIBC patients were included in the study. RNA was extracted from urinary cells and expression of 8 microRNAs, previously described by our group, was analysed by quantitative PCR. A tumour progression predicting model was developed by Cox regression analysis and validated by bootstrapping. Regression analysis identified miR-140-5p and miR-92a-3p as independent predictors of tumour progression. The risk score derived from the model containing these two microRNAs was able to discriminate between two groups with a highly significant different probability of tumour progression (HR, 5.204; p<0.001) which was maintained when patients were stratified according to tumour risk. The algorithm was also able to identify two groups with different cancer-specific survival (HR, 3.879; p=0.021). Although the data needs to be externally validated, miRNA analysis in urine appears to be a valuable prognostic tool in NMIBC patients.

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“…PTEN may regulate PI3K signaling by dephosphorylating the lipid signaling intermediate phosphatidylinositol (3,4,5)-trisphosphate, and a clear link between the PI3K pathway and cancer was established in the 1980s (32). miRNA always operated by binding to the 3'UTRs of their target genes and a number of previous reports have confirmed that miR-106b serves its part in colorectal cancer, gastric cancer and hepatocellular carcinoma (33,34). In the present study, it was demonstrated that miR-106b inhibition may result in the increased expression of PTEN in ESCC cells compared with those in control cells.…”

Section: Downregulation Of Pten Partially Rescued the Induction Of Thmentioning

confidence: 99%

miR-106b promotes cell invasion and metastasis via PTEN mediated EMT in ESCC

et al. 2018

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Abstract. MicroRNA (miR)-106b serves an essential function in a variety of human cancer types, particularly in the process of invasion and metastasis. However, the function and mechanism of miR-106b in the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) has remained elusive. In the present study, it was demonstrated that miR-106b was upregulated in ESCC tissues and cell lines. Furthermore, miR-106b expression in ESCC tissues was positively associated with lymphatic metastasis. Inhibition of miR-106b in EC-1 and EC9706 cells decreased not only the invasion and metastasis ability but also the proliferation ability of EC-1 and EC9706 cells. In addition, miR-106b had the ability to induce epithelial-to-mesenchymal transition (EMT) in EC-1 and EC9706 cells. In terms of the underlying mechanism, it was revealed that miR-106b promoted the invasion, metastasis and proliferation ability of EC-1 and EC9706 cells by directly targeting phosphatase and tension homolog (PTEN). Furthermore, miR-106b induced EMT in EC-1 and EC9706 cells by suppressing the expression of PTEN. In summary, the present study revealed that miR-106b contributed to invasion and metastasis in ESCC by regulating PTEN mediated EMT. Downregulation of miR-106b may be a novel strategy for preventing tumor invasion and metastasis. IntroductionEsophageal squamous cell carcinoma (ESCC) is the most malignant lesion in China, particularly in Linzhou, Henan (1).Treatment of ESCC is largely useless due to the occurrence of invasion and metastasis in the early stage. However, the mechanism of invasion and metastasis of ESCC has been poorly elucidated (2).Epithelial-to-mesenchymal transition (EMT) now is always viewed as a key event that occurs during cancer invasion and metastasis. However, current understanding of the alterations that give rise to the occurrence of EMT is limited. MicroRNAs (miRNA/miRs) are small non-coding RNA molecules that may directly regulate target gene expression by binding to their 3'-untranslated regions (3'-UTRs) (3,4). Furthermore, miRNAs have been demonstrated to serve notable functions in tumor invasion and metastasis by functioning as EMT suppressors or inducers (5,6). miR-106b is a type of miRNA transcribed from the miR-106b-25 cluster located on chromosome 7 (7). Yau et al (8) reported that miR-106b overexpressed in hepatocellular carcinoma cells and that the overexpression of miR-106b may promote cell migration and metastasis by activating the EMT process. Zhou et al (9) additionally demonstrated that miR-106b contributed as an EMT inducer in breast cancer. However, whether miR-106b participates in the invasion and metastasis process of ESCC by inducing EMT and the mechanism of how miR-106b induces EMT in ESCC had not been fully explored until now. miRNAs participate in the occurrence and development of a cancer by regulating the post-transcriptional process of their target gene. Several genes have been verified to be the targets of miR-106b, including transforming growth factor-β type II receptor, cyclin de...

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MicroRNA-92a promotes growth, metastasis, and chemoresistance in non-small cell lung cancer cells by targeting PTEN

Cited by 70 publications

References 44 publications

A panel of microRNA signature in serum for colorectal cancer diagnosis

A panel of microRNA signature in serum for colorectal cancer diagnosis

Urinary cell microRNA-based prognostic classifier for non-muscle invasive bladder cancer

miR-106b promotes cell invasion and metastasis via PTEN mediated EMT in ESCC

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