MicroRNA-92a Functions as an Oncogene in Colorectal Cancer by Targeting PTEN

Zhang, Guangjun; Zhou, He; Xiao, Hua-xu; Liu, Zuoliang; Tian, Hongpeng; Zhou, Tong

doi:10.1007/s10620-013-2858-8

Cited by 113 publications

(91 citation statements)

References 30 publications

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“…However, other studies demonstrated that miR-92a expression is upregulated in several cancers and functions as oncogene and plays a critical role in cancer development. For example, Zhang et al reported that miR-92a induced EMT and regulated cell growth, migration, and invasion in the colorectal cancer cells, at least in part, via suppression of PTEN expression [28]. Chen et al found that miR-92a expression was increased in esophageal squamous cell carcinoma (ESCC), and its expression was significantly associated with the lymph node metastasis and TNM stage in ESCC patients and promoted the migration and invasion of ESCC cells via targeting CDH1 [29].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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MicroRNA-92a (miR-92a) has been reported to play important roles in tumorigenesis of human various cancers. However, the roles and underlying molecular mechanism of miR-92a in non-small cell lung cancer (NSCLC) have not been totally elucidated. Therefore, the aims of this study were to determine the role of miR-92a and to elucidate its regulatory mechanism in NSCLC. We found that miR-92a was significantly upregulated in NSCLC tissues compared to matched adjacent normal lung tissues, and its expression is significantly associated with clinical characteristics of patients, including tumor, node, and metastasis (TNM) stage; tumor size; and lymph node metastasis (all P < 0.01). Function assays demonstrated that upregulation of miR-92a in NSCLC cells promoted cell proliferation, migration, and invasion, decreased apoptosis and caspase-3 activity, and enhanced chemoresistance of NSCLC cells, whereas downregulation of miR-92a showed the opposite effects. Moreover, phosphatase and tensin homolog (PTEN), a unique tumor suppressor gene, was confirmed as a direct target of miR-92a, and PTEN messenger RNA (mRNA) expression was decreased in NSCLC tissues and was inversely correlated with miR-92a. Downregulation of PTEN could mimic the same effects of miR-92a mimic in NSCLC cells and rescue the effects on NSCLC cells induced by miR-92a inhibitor. Taken together, these findings suggested that miR-92a could promote growth, metastasis, and chemoresistance in NSCLC cells at least partially by targeting PTEN.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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“…This agreed with Faltejskova et al [33] who documented evidence against using it in diagnosing and monitoring CRC, contrary to many studies that confirmed its significant role in diagnosing CRC with adequate sensitivity and specificity [11,34,[37][38][39]. Even Huang et al ascertained its role when combined with miR-29a [34].…”

Section: Discussionsupporting

confidence: 73%

“…miR-29a promoted CRC and its metastasis by regulating matrix metalloproteinase and E-cadherin, through its direct targeting KLF4 [9], the identified tumour suppressor gene involved in cell proliferation, migration and invasion [10]. Similarly, miR92a, which was upregulated in CRC, stimulated epithelial to mesenchymal transition, with negative influence on phosphatase and tensin homologue lucoferase activity [11]. On the contrary, miRNA-145 was downregulated in most primary CRC, particularly the aggressive forms, via targeting fascin-1 [12], elementary in neoangiogenesis [13].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of microRNAs-29a, 92a and 145 in colorectal carcinoma as candidate diagnostic markers: An Egyptian pilot study

Ramzy

Hasaballah

Marzaban

et al. 2015

Clinics and Research in Hepatology and Gastroenterology

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“…The aberrant expression of many miRNAs has been linked to human diseases including cancers. 7 To date, multiple cellular miRNAs, such as miR-148a, 8 miR-155, 9 miR-377, 10 miR-92a, 11 miR-200c, 12 miR-23a, 13 miR-130b, 14 miR-30a, 15 miR-149 16 and miR-93 17 have been reported to modulate the EMT and metastasis in various cancers, but only three of them are implicated in the EMT in nasopharyngeal carcinoma (NPC), a malignancy typically featured by its early metastasis and invasion. [17][18][19] Therefore, it is necessary to identify other unknown miRNAs that regulate the EMT and metastasis of NPC cells.…”

Section: Introductionmentioning

confidence: 99%

EBV-miR-BART7-3p promotes the EMT and metastasis of nasopharyngeal carcinoma cells by suppressing the tumor suppressor PTEN

et al. 2014

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The epithelial-mesenchymal transition (EMT) is crucial to cancer progression and metastasis. Although multiple cellular miRNAs have been identified to regulate the EMT and metastasis in cancers, the role of viral miRNAs in cancer progression remains largely unknown. Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus (EBV)-associated malignancy typically characterized by its early metastasis. In the present study, we have discovered the involvement of a viral miRNA, EBV-miR-BART7-3p, in the EMT and metastasis of NPC cells. Initially, we observed that EBV-miR-BART7-3p was highly expressed in NPC and positively correlated with lymph node metastasis and clinical stage of NPC. Subsequently, we demonstrated that EBV-miR-BART7-3p enhanced cell migration/invasion in vitro, cancer metastasis in vivo, and particularly the EMT characterized by loss of epithelial markers and gain of mesenchymal features in NPC cells. Furthermore, mechanistic studies disclosed that EBV-miR-BART7-3p targeted a major human tumor suppressor PTEN, modulating PI3K/Akt/GSK-3β signaling and eventually leading to the high expression and nuclear accumulation of Snail and β-catenin, which favor EMT. Knockdown of PTEN could phenocopy the effect of EBV-miR-BART7-3p, whereas re-expression of PTEN resulted in a phenotypic reversion. Moreover, these findings were supported by an observation of an EBV-positive cell model in which silencing of endogenous EBV-miR-BART7-3p partially attenuated cell migration/invasion and altered EMT protein expression pattern via reverting PI3K/Akt, Snail and β-catenin expression. Thus, this study suggests a novel mechanism by which EBV-miR-BART7-3p modulates the EMT and metastasis of NPC cells, and a clinical implication of EBV-miR-BART7-3p as a potential biomarker or therapeutic target.

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MicroRNA-92a Functions as an Oncogene in Colorectal Cancer by Targeting PTEN

Abstract: Our results demonstrated that miR-92a induced EMT and regulated cell growth, migration and invasion in the SW480 cells, at least partially, via suppression of PTEN expression. MiR-92a may serve as a novel therapeutic target in colorectal cancer.

Cited by 113 publications

References 30 publications

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

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

Evaluation of microRNAs-29a, 92a and 145 in colorectal carcinoma as candidate diagnostic markers: An Egyptian pilot study

EBV-miR-BART7-3p promotes the EMT and metastasis of nasopharyngeal carcinoma cells by suppressing the tumor suppressor PTEN

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