Integrative transcriptome analysis identifies deregulated microRNA-transcription factor networks in lung adenocarcinoma

Cinegaglia, Naiara da Costa; Andrade, Sónia C. S.; Tokár, Tomáš; Pinheiro, Maísa; Severino, Fabio; Oliveira, Rogério Antônio de; Hasimoto, Érica Nishida; Catâneo, Daniele Cristina; Catâneo, Antônio José Maria; Defaveri, Júlio; Souza, Cleonilson Protásio de; Marques, Márcia Maria Chiquitelli; Carvalho, Robson Francisco; Coutinho, Luiz Lehmann; Gross, Jefferson Luiz; Rogatto, Sílvia Regina; Lam, Wan L.; Jurišica, Igor; Reis, Patrícia P.

doi:10.18632/oncotarget.8713

Cited by 46 publications

(38 citation statements)

References 79 publications

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“…25 Many research have showed that miR-1247-5p was downregulated in cancer tissues, and it act as a tumour inhibition factor. 16,[26][27][28] In accord with the above results, our study suggested that miR-1247-5p was downregulated in BC tissues relative to cancer free tissues, indicating that downregulation of miR-1247-5p expression was associated with carcinogenesis and cancer development of BC.…”

Section: Discussionsupporting

confidence: 85%

“…A systematic review showed that two candidate microRNAs (miR‐21 and miR‐210) were upregulated and six microRNAs (miR‐99a, miR‐139‐5p, miR‐145, miR‐195, miR‐205 and miR‐497) were downregulated in BC tissues comparing with normal tissues . Many research have showed that miR‐1247‐5p was downregulated in cancer tissues, and it act as a tumour inhibition factor . In accord with the above results, our study suggested that miR‐1247‐5p was downregulated in BC tissues relative to cancer free tissues, indicating that downregulation of miR‐1247‐5p expression was associated with carcinogenesis and cancer development of BC.…”

Section: Discussionsupporting

confidence: 85%

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Association of miR‐1247‐5p expression with clinicopathological parameters and prognosis in breast cancer

Zhang

Fan

et al. 2018

Int J Experimental Path

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SummaryOur study aimed to clarify the correlation between miR‐1247‐5p expression and clinicopathological parameters and survival of patients with breast cancer (BC). We evaluated the expression level of miR‐1247‐5p in 224 formalin‐fixed, paraffin‐embedded specimens (112 BC and matched cancer free tissues) by quantitative real‐time reverse transcriptase polymerase chain reaction (qRT‐PCR). miR‐1247‐5p expression in BC tissues was found to be decreased compared with matched normal tissues (P < 0.01). Additionally, low miR‐1247‐5p expression in BC tissues was significantly associated with the advanced TNM stage (P = 0.007), lymph node metastasis (P = 0.015), poorer pathological differentiation (P = 0.005) and molecular subtype (P = 0.027). The patients in the low miR‐1247‐5p group had a shorter disease‐free survival and overall survival than those in the high miR‐1247‐5p group (P < 0.01). Furthermore, the univariate and the multivariate analyses showed that miR‐1247‐5p expression was an independent predictor of overall survival (P < 0.01). Our study showed that miR‐1247‐5p was related to the biological behaviour of breast tumour and prognosis of patients with BC. miR‐1247‐5p could be a novel tumour suppressor and act as a potential biomarker and therapeutic agent for breast carcinoma.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionsupporting

confidence: 85%

Association of miR‐1247‐5p expression with clinicopathological parameters and prognosis in breast cancer

Zhang

Fan

et al. 2018

Int J Experimental Path

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“…(22) In addition, as well as miR181-a and miR-181b, miR-181c, which has been shown to promote pancreatic cancer cell chemoresistance, (23) are aberrantly expressed in various cancers, including osteosarcoma and lung adenocarcinoma. (18,24) These findings raise the possibility that miR-181b and miR-181c have a similar function to miR-181a in HCC cells. In addition, Ji et al (16) indicate that all members of miR-181s are associated with HCC cells with features of hepatic cancer stem cells, suggesting that HepG2 cells, which have mature features of HCC cells, express lower levels of miR-181s.…”

Section: Discussionmentioning

confidence: 92%

“…We showed that miR‐181a directly represses expression of RASSF1 in HCC cells, which is consistent with a recent report that miR‐181a and miR‐181b are highly expressed in acute promyelocytic leukemia and downregulate RASSF1 expression . In addition, as well as miR181‐a and miR‐181b, miR‐181c, which has been shown to promote pancreatic cancer cell chemoresistance, are aberrantly expressed in various cancers, including osteosarcoma and lung adenocarcinoma . These findings raise the possibility that miR‐181b and miR‐181c have a similar function to miR‐181a in HCC cells.…”

Section: Discussionmentioning

confidence: 99%

miR‐181a induces sorafenib resistance of hepatocellular carcinoma cells through downregulation of RASSF1 expression

et al. 2016

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Sorafenib, a multi‐kinase inhibitor, is the only standard clinical drug for patients with advanced hepatocellular carcinoma (HCC); however, development of sorafenib resistance in HCC often prevents its long‐term efficacy. Therefore, novel targets and strategies are urgently needed to improve the antitumor effect of sorafenib. In the present study, we examined the novel mechanisms of sorafenib resistance of HCC cells by investigating the difference in sorafenib sensitivity between two HCC cell lines. Sorafenib induced more apoptosis of HepG2 cells compared to Hep3B cells. Sorafenib exposure to HepG2 cells but not Hep3B cells increased the expression of proapoptotic factor PUMA, and activated PARP and caspase‐3. Notably, microRNA‐181a (miR‐181a) expression levels were lower in HepG2 cells than in Hep3B cells. Exogenous miR‐181a expression in HepG2 cells reduced apoptosis, whereas inhibition of miR‐181a in Hpe3B cells increased apoptosis. In addition, we demonstrated that miR‐181a directly targets RASSF1, a MAPK signaling factor, and knockdown of RASSF1 increased sorafenib resistance. Taken together, these results suggest that miR‐181a provokes sorafenib resistance through suppression of RASSF1. Our data provide important insight into the novel therapeutic strategy against sorafenib resistance of HCC cells by targeting of miR‐181a pathway.

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“…9 miR-421 expression was also screened to be higher in lung adenocarcinoma tissues in comparison to adjacent normal tissues. 10 miR-421, located at the Xq13.2 region of the X chromosome, is closely related to the checkpoint changes of S-phase cell cycle and increased sensitivity to ionizing radiation through its ectopic expression. 11 miR-421 has been reported to negatively target caspase-3 at the posttranscriptional level, as well as to regulate Bcl-2-Associated X protein (Bax) and Bcell lymphoma-2 (Bcl-2), ultimately highlighting its role as a tumor promoter in gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐421 inhibition alleviates bronchopulmonary dysplasia in a mouse model via targeting Fgf10

Yuan

Daiqun

Huang

et al. 2019

J of Cellular Biochemistry

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Bronchopulmonary dysplasia (BPD) is a common and refractory disease affecting newborn children and infants with alveolar dysplasia and declined pulmonary function. Several microRNAs (miRNAs) have been found to be differentially expressed in BPD progression. This study further explores the role of miR‐421 via fibroblast growth factor 10 (Fgf10) in mice with BPD. A mouse model of BPD was established through the induction of hyperoxia, in which the expression pattern of miR‐421 and Fgf10 was identified. Furthermore, adenovirus‐packed vectors were injected in mice to intervene miR‐421 and Fgf10 expression, including miR‐421 mimics or inhibitors, and si‐Fgf10 to explore the role of miR‐421 and Fgf10 in BPD. The target relationship between miR‐421 and Fgf10 was investigated. Inflammatory response and cell apoptosis were observed in the mice, with inflammatory cytokines and apoptosis‐related factors detected by applying Reverse transcription quantitative polymerase chain reaction, Western blot analysis, and enzyme‐linked immunosorbent assay. Fgf10 was confirmed as a target gene of miR‐421. Elevated expression of miR‐421 was evident, while Fgf10 was poorly expressed in BPD. upregulation of miR‐421 and silence of Fgf10 aggravated inflammatory response in lung tissue and promoted lung cell apoptosis in BPD. The aforementioned alterations could be reversed by downregulation of miR‐421. Collectively, inhibition of miR‐421 can assist in the development of BPD in mice BPD by upregulating Fgf10. Therefore, the present study provides a probable target for the treatment of BPD.

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Integrative transcriptome analysis identifies deregulated microRNA-transcription factor networks in lung adenocarcinoma

Cited by 46 publications

References 79 publications

Association of miR‐1247‐5p expression with clinicopathological parameters and prognosis in breast cancer

Association of miR‐1247‐5p expression with clinicopathological parameters and prognosis in breast cancer

miR‐181a induces sorafenib resistance of hepatocellular carcinoma cells through downregulation of RASSF1 expression

MicroRNA‐421 inhibition alleviates bronchopulmonary dysplasia in a mouse model via targeting Fgf10

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