MiR-140-3p suppressed cell growth and invasion by downregulating the expression of ATP8A1 in non-small cell lung cancer

Wang, Dong; Yao, Chunping; Teng, Xuepeng; Chai, Jie; Yang, Xinhua; Li, Baosheng

doi:10.1007/s13277-015-3452-9

Cited by 62 publications

(44 citation statements)

References 53 publications

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“…Collectively, the key findings in this study support the notion that miR-140-3p plays an important role in HCC progression, providing evidence for the mechanism that miR-140-3p-targeted GRN inhibition mediates the MAPK signaling pathway, by The first main finding of our study was that miR-140-3p was under-expressed in HCC and GRN upregulated in HCC. Importantly, miR-140-3p has been identified as a downregulated miRNA in most cancers, such as non-small cell lung cancer, 27 and basal-like early-stage breast cancer. 28 Apart from that, miR-140 is the most stable miRNA in HCC samples.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Upregulation of microRNA‐140‐3p inhibits epithelial‐mesenchymal transition, invasion, and metastasis of hepatocellular carcinoma through inactivation of the MAPK signaling pathway by targeting GRN

Zhang

Men

Ding

2019

J of Cellular Biochemistry

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Invasion and metastasis in hepatocellular carcinoma (HCC) results in poor prognosis. Human intervention in these pathological processes may benefit the treatment of HCC. The aim of the present study is to elucidate the mechanism of miR‐140‐3p affecting epithelial‐mesenchymal transition (EMT), invasion, and metastasis in HCC. Microarray analysis was performed for differentially expressed genes screening. The target relationship between miR‐140‐3p and GRN was analyzed. Small interfering RNA (siRNA) against granulin (GRN) was synthesized. EMT markers were detected, and invasion and migration were evaluated in HCC cells introduced with a miR‐140‐3p inhibitor or mimic, or siRNA against GRN. A mechanistic investigation was conducted for the determination of mitogen‐activated protein kinase (MAPK) signaling pathway‐related genes and EMT markers (E‐cadherin, N‐cadherin, and Vimentin). GRN was highlighted as an upregulated gene in HCC. GRN was a target gene of miR‐140‐3p. Elevation of miR‐140‐3p or inhibition of GRN restrained the EMT process and suppressed the HCC cell migration and invasion. HCC cells treated with the miR‐140‐3p mimic or siRNA‐GRN exhibited decreased GRN expression and downregulated the expressions of the MAPK signaling pathway‐related genes, N‐cadherin, and Vimentin but upregulated the expression of E‐cadherin. GRN silencing can reverse the activation of the MAPK signaling pathway and induction of EMT mediated by miR‐140‐3p inhibition. Taken together, the results show that miR‐140‐3p confers suppression of the MAPK signaling pathway by targeting GRN, thus inhibiting EMT, invasion, and metastasis in HCC.

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Section: Discussionmentioning

confidence: 99%

Retracted: Upregulation of microRNA‐140‐3p inhibits epithelial‐mesenchymal transition, invasion, and metastasis of hepatocellular carcinoma through inactivation of the MAPK signaling pathway by targeting GRN

Zhang

Men

Ding

2019

J of Cellular Biochemistry

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“…Ren et al () showed that miRNA‐92a promotes growth in NSCLC cells via targeting PTEN. In addition, miR‐140‐3p suppressed cell growth and invasion by downregulating the expression of ATP8A1 in NSCLC (Dong et al, ). For another, several miRNAs serve as oncogenes in NSCLC (Ye et al, ; Yu et al, ).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐455 suppresses non‐small cell lung cancer through targeting ZEB1

Chen

Tang

et al. 2016

Cell Biology International

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MicroRNA-455 (miRNA-455), which is downregulated in human cancer, potently mediates the multiple steps of carcinogenesis. However, the role of miR-455 in non-small cell lung cancer (NSCLC) carcinogenesis remains unclear. In present study, we determined the mature miRNA-455 expression in NSCLC tissues and cells by real-time PCR. Follow-up studies examined the effects of a miR-455 mimic (gain of function) on cell proliferation, migration, and invasion. Our data indicate that miR-455 was significantly down-regulated in NSCLC cell lines and tissues. In functional assays, overexpression of miR-455 suppressed the proliferation, migration, and invasion of NSCLC cell lines. Data from reporter assays showed that miR-455 directly binds to 3'UTR of ZEB1 and suppresses the endogenous level of ZEB1 protein expression. Furthermore, overexpression of ZEB1 reverses miR-455-suppressed malignant phenotype of NSCLC cells. Moreover, we found that upregulation of ZEB1 expression is inversely associated with miR-455 expression in NSCLC tissues. Taken together, miR-455 as an anti-oncogene in non-small cell lung cancer through up-regulation of ZEB1 and serve as a potential therapeutic target in NSCLC.

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“…This protein is a human tumor suppressor that accounts for the majority of cellular serine/threonine phosphatase activity [40]. ATP8A1 is a member of P4-ATPase family with a role in the formation of membrane ruffles to promote cell migration [41]. BLPAP (Bladder cancer-associated protein) is a highly conserved protein among species displaying tissue-specific expression patterns, but also tissue-specific functions being both a tumor suppressor and a tumor promoting [42].…”

Section: Resultsmentioning

confidence: 99%

Candidate genes and pathways downstream of PAX8 involved in ovarian high-grade serous carcinoma

et al. 2016

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Understanding the biology and molecular pathogenesis of ovarian epithelial cancer (EOC) is key to developing improved diagnostic and prognostic indicators and effective therapies. Although research has traditionally focused on the hypothesis that high-grade serous carcinoma (HGSC) arises from the ovarian surface epithelium (OSE), recent studies suggest that additional sites of origin exist and a substantial proportion of cases may arise from precursor lesions located in the Fallopian tubal epithelium (FTE). In FTE cells, the transcription factor PAX8 is a marker of the secretory cell lineage and its expression is retained in 96% of EOC. We have recently reported that PAX8 is involved in the tumorigenic phenotype of ovarian cancer cells. In this study, to uncover genes and pathways downstream of PAX8 involved in ovarian carcinoma we have determined the molecular profiles of ovarian cancer cells and in parallel of Fallopian tube epithelial cells by means of a silencing approach followed by an RNA-seq analysis. Interestingly, we highlighted the involvement of pathways like WNT signaling, epithelial-mesenchymal transition, p53 and apoptosis. We believe that our analysis has led to the identification of candidate genes and pathways regulated by PAX8 that could be additional targets for the therapy of ovarian carcinoma.

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MiR-140-3p suppressed cell growth and invasion by downregulating the expression of ATP8A1 in non-small cell lung cancer

Cited by 62 publications

References 53 publications

Retracted: Upregulation of microRNA‐140‐3p inhibits epithelial‐mesenchymal transition, invasion, and metastasis of hepatocellular carcinoma through inactivation of the MAPK signaling pathway by targeting GRN

Retracted: Upregulation of microRNA‐140‐3p inhibits epithelial‐mesenchymal transition, invasion, and metastasis of hepatocellular carcinoma through inactivation of the MAPK signaling pathway by targeting GRN

MicroRNA‐455 suppresses non‐small cell lung cancer through targeting ZEB1

Candidate genes and pathways downstream of PAX8 involved in ovarian high-grade serous carcinoma

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