RETRACTED: MicroRNA-19a and -19b regulate cervical carcinoma cell proliferation and invasion by targeting CUL5

Xu, Xue Mei; Wang, Xiao Bo; Chen, Miao Miao; Liu, Tao; Li, Yi Xuan; Jia, Wei Hua; Liu, Min; Li, Xin; Tang, Hua

doi:10.1016/j.canlet.2012.02.038

Cited by 109 publications

(94 citation statements)

References 33 publications

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“…36 Recent studies have shown that miR-19a and miR-19b-1 promoted the migration of cervical carcinoma cells 16 and colon cancer cells. 17 In addition, it has been reported that miR-19a/b facilitated the migration, invasion, and metastasis of gastric cancer cells by targeting the tumour suppressor MXD1. 14 miR-19 overexpression induces EMT of lung cancer cells J Li et al Furthermore, Fan et al 18 reported that miR-19b promoted the migration, invasion, and metastasis of Hela, MCF7, and Huh7 cells by targeting TP53.…”

Section: Discussionmentioning

confidence: 99%

“…It seems that the proliferation inhibition of miR-19 in lung cancer cells is inconsistent with its oncogene role. 1,5,6,10,16,17,29 It has been reported that EMT contributed to the invasion and migration of tumor cells, and EMT was attributed to the metastatic dissemination and the resistance of tumor cells to radiotherapy, chemotherapy, and apoptosis. 19,32,39 Tumor cells undergoing EMT are typically found at the edge of tumors, account for a small proportion of primary cancer, and have low proliferative rates.…”

Section: Discussionmentioning

confidence: 99%

“…12,13 In a mouse model of c-Myc-driven B-cell lymphomas, Em-myc/miR-19b-1 lymphomas are highly invasive as lymphoma cells invaded the thymus and bone marrow, as well as visceral organs outside the lymphoid compartment, including the liver, lung, and, occasionally, the kidney. 10 More recent studies have reported that miR-19a or miR-19b-1 promoted the migration and invasion of cervical carcinoma cells, 16 colon cancer cells, 17 and gastric cancer cells through targeting the tumor suppressor MXD1, 14 and Hela, MCF7, and Huh7 cells through targeting TP53. 18 Taken together, these results support that miR-19 is involved in cancer invasion and metastasis; however, the underlying mechanisms remain largely unknown.…”

mentioning

confidence: 99%

“…Given that miR-19 is associated with cancer invasion and metastasis and EMT is the central mechanism underlying cancer invasion and metastasis, [10][11][12][13][14][15][16][17][18] the present study aimed to investigate whether miR-19 is able to induce EMT and enhance invasion and metastasis of human cancer cells. Our results showed that enforced expression of miR-19 in lung cancer cells induced EMT, which caused growth inhibition but elevated migration of the cancer cells.…”

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confidence: 99%

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MicroRNA-19 triggers epithelial–mesenchymal transition of lung cancer cells accompanied by growth inhibition

Yang

Yan

et al. 2015

Laboratory Investigation

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The miR-19 family (miR-19a and miR-19b-1) are key oncogenic components of the miR-17-92 cluster. Overexpression of miR-19 is strongly associated with cancer invasion and metastasis, and poor prognosis of cancer patients. However, the underlying mechanisms remain largely unknown. In the present study, we found that enforced expression of miR-19 including miR-19a and miR-19b-1 triggered epithelial-mesenchymal transition (EMT) of lung cancer cells A549 and HCC827 as shown by mesenchymal-like morphological conversion, downregulation of epithelial proteins (e.g., E-cadherin, ZO-1 (zona occludens 1), and α-catenin), upregulation of mesenchymal proteins (e.g., vimentin, fibronectin 1, N-cadherin, and snail1), formation of stress fibers, and reduced cell adhesion. In addition, enhanced migration and invasion were observed in the cancer cells A549 and HCC827 undergoing EMT. In contrast, silencing of endogenous miR-19 reversed EMT and reduced the migration and invasion abilities of A549 and HCC827 cells. DNA microarray results revealed significant changes of the expression of genes related to EMT, migration, and metastasis of miR-19-expressing A549 cells. Moreover, siRNA-mediated knockdown of PTEN, a target of miR-19, also resulted in EMT, migration, and invasion of A549 and HCC827 cells, suggesting that PTEN is involved in miR-19-induced EMT, migration and invasion of lung cancer cells. Furthermore, lung cancer cells undergoing EMT induced by miR-19 demonstrated reduced proliferation in vitro and in vivo, and enhanced resistance to apoptosis caused by TNF-α. Taken together, these findings suggest that miR-19 triggers EMT, which has an important role in the invasion and migration of lung cancer cells, accompanied by the reduced proliferation of cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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MicroRNA-19 triggers epithelial–mesenchymal transition of lung cancer cells accompanied by growth inhibition

Yang

Yan

et al. 2015

Laboratory Investigation

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“…Also, our studies were performed using qRT-PCR-based techniques, which have already been demonstrated as powerful tools for microRNA quantification as they allow good sensitivity and specificity (28). Moreover, the reliability of TLDA method is based on the presence of specific forward PCR primer and TaqMan probes and it relies on qRT-PCR, the gold standard method for expression analysis (44,45).…”

Section: Discussionmentioning

confidence: 99%

microRNA Portraits in Human Vulvar Carcinoma

Maia

Lavorato-Rocha

Rodrigues

et al. 2013

Cancer Prevention Research

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Unregulated expression of microRNAs is well known and has already been demonstrated in many tumor types. However, in vulvar carcinoma this field has been unknown territory. Our study characterizes microRNA in vulvar tumors through an expression profile of 754 miRNAs, relating this with clinical and anatomopathologic data, and presence of HPV infection. Twenty HPV-negative and 20 HPV-positive samples, genotyped for high-risk HPVs (HPV16, 18, 31, 33) and a pool of seven normal vulvar skin samples were used for the identification of differentially expressed miRNAs by TLDA Quantitative Real Time PCR (qRT-PCR). Twenty-five differentially expressed microRNAs between HPV-positive and HPV-negative groups and 79 differentially expressed on the tumor compared with normal samples were obtained. A network between microRNA expression profiles and putative target mRNAs predicted by target prediction algorithms and previously demonstrated as relevant in vulvar carcinomas, such as TP53, RB, PTEN, and EGFR was constructed. Downregulation of both miR-223-5p and miR-19-b1-5p were correlated with the presence of lymph node metastasis; downregulation of miR-100-3p and miR-19-b1-5p were correlated with presence of vascular invasion; overexpression of miR-519b and miR-133a were associated with advanced FIGO staging. In conclusion, our study demonstrates that microRNAs may be clinically important in vulvar carcinomas and our findings may help for further studies on functional implications of miRNA deregulation in this type of cancer. Cancer Prev Res; 6(11); 1231-41. Ó2013 AACR.

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The STAT3‐miR‐223‐TGFBR3/HMGCS1 axis modulates the progression of cervical carcinoma

Jiang

Qian

et al. 2020

Molecular Oncology

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Cervical cancer is induced by persistent infections with high‐risk human papillomaviruses (HPVs), which produce the early protein 6 of HPVs (E6)/E7 protein that is involved in cell transformation by interacting with several oncoproteins or tumor suppressors. However, the role of noncoding RNA in mediating the pathogenesis of cervical cancer remains unclear. Here, we report that the novel signal transducer and activator of transcription 3 (STAT3)‐microRNA‐223‐3p (miR‐223)‐TGFBR3/HMGCS1 axis regulated by the E6 protein controls cervical carcinogenesis. miR‐223 was highly expressed in cervical tumor tissues, whereas TGFBR3 or HMGCS1 was significantly downregulated. miR‐223 targeted the 3′‐UTRs of TGFBR3 and HMGCS1 and suppressed their expression, leading to increased anchorage‐independent growth and cervical squamous cell carcinoma (CSCC) tumor growth in vitro and in vivo. The increased expression of miR‐223 was mediated by the transcription factor STAT3, whose activity was enhanced by E6 in the context of interleukin (IL)‐6 stimulation. In addition, exosomal miR‐223 derived from CSCC cells induced IL‐6 secretion by monocyte/macrophage in a coculture system in vitro, and IL‐6 secretion, in turn, led to enhanced STAT3 activity in CSSC cells, forming a positive feedback loop. Furthermore, modified miR‐223 inhibitor effectively suppressed tumor growth in cell line‐derived xenograft model, suggesting that miR‐223 is a potential promising therapeutic target in CSCC. In conclusion, our results demonstrate that the STAT3‐miR‐223‐HMGCS1/TGFBR3 axis functions as a key signaling pathway in cervical cancer progression and provides a new therapeutic target.

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RETRACTED: MicroRNA-19a and -19b regulate cervical carcinoma cell proliferation and invasion by targeting CUL5

Cited by 109 publications

References 33 publications

MicroRNA-19 triggers epithelial–mesenchymal transition of lung cancer cells accompanied by growth inhibition

MicroRNA-19 triggers epithelial–mesenchymal transition of lung cancer cells accompanied by growth inhibition

microRNA Portraits in Human Vulvar Carcinoma

The STAT3‐miR‐223‐TGFBR3/HMGCS1 axis modulates the progression of cervical carcinoma

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