Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer

Wang, Shou-Hua; Ma, Fei; Tang, Zhaohui; Wu, Xiaodi; Cai, Qiang; Zhang, Mingdi; Weng, Mingzhe; Zhou, Di; Wang, Jiandong; Quan, Zhiwei

doi:10.1186/s13046-016-0436-6

Cited by 109 publications

(89 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…On the contrary, Yu et al reported that H19 potentiated choriocarcinoma cell apoptosis [12]. In our study H19 inhibited apoptosis and promoted the proliferation of gastric cancer cells, which is consistent with other recent studies [23-25]. It has been established that miR-675 derives from the firs exon of H19, and miR-675 has been reported as being at least partially responsible for the regulation of H19 function [26, 27].…”

Section: Discussionsupporting

confidence: 82%

“…Therefore, our data demonstrate that H19/miR-675 could target FADD, increase pro-caspase 8/3, and inhibit apoptosis. In addition to H19/miR-675 axis, H19 also can regulate tumorigenesis through other mechanisms involving other H19 exons besides the first one [37, 38]. Therefore the analysis of the function of H19 with mutation in the exon 1 is needed in the future to illuminate possible new mechanisms and ruling out the effect of miR-675.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Yan¹,

Zhang²,

Qiang³

et al. 2017

Cell Physiol Biochem

109

View full text Add to dashboard Cite

Background: Long noncoding RNA (lncRNA) H19 is emerging as a vital regulatory molecule in the progression of different types of cancer and miR-675 is reported to be embedded in H19's first exon. However, their function and specific mechanisms of action have not been fully elucidated. The aim of this study was to identify a novel lncRNA-microRNA-mRNA functional network in gastric cancer. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the relative expression of H19 and miR-675 in normal (GES-1) and gastric cancer cell lines (SGC-7901, SGC-7901/DDP) as well as in tumor tissues. Gain and loss of function approaches were carried out to investigate the potential roles of H19/miR-675 in cell proliferation and apoptosis. Moreover, Fas associated via death domain (FADD) was validated to be the target of miR-675 via luciferase reporter assay. Western blotting was used to evaluate the protein expression of related signaling pathway. Results: In our study H19 and miR-675 were increased in gastric cancer cell lines and tissues. Overexpression of H19 and miR-675 promoted cell proliferation and inhibited cell apoptosis, whereas knockdown of H19 and miR-675 inhibited these effects. By further examining the underlying mechanism, we showed that H19/miR-675 axis inhibited expression of FADD. FADD downregulation subsequently inhibited the caspase cleavage cascades including caspase 8 and caspase 3. Conclusion: Taken together, our results point to a novel regulatory pathway H19/miR-675/ FADD/caspase 8/caspase 3 in gastric cancer which may be potential target for cancer therapy.

show abstract

Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Yan¹,

Zhang²,

Qiang³

et al. 2017

Cell Physiol Biochem

109

View full text Add to dashboard Cite

show abstract

“…None of these associations, however, have been reported in the literature. On the other hand, studies have demonstrated hits on the gene regulation between hsa-miR-142-5p and CD24 [86], hsa-miR-29 and DNMT3B [87, 88], hsa-miR-142-3p and EGR2 [89], hsa-miR-150 and EGR2 [90], hsa-miR-34a and IKZF3 [91], hsa-miR-150 and MIAT [92], hsa-miR-342-3p and PSMG3 [93, 94], hsa-miR-17 and TIMP3 [95]. Our results further suggested an important correlation between miRNAS and gene expression values in both Basal I and Basal II, identified by this in silico approach.…”

Section: Discussionmentioning

confidence: 99%

Basal-like breast cancer: molecular profiles, clinical features and survival outcomes

et al. 2017

View full text Add to dashboard Cite

BackgroundBasal-like constitutes an important molecular subtype of breast cancer characterised by an aggressive behaviour and a limited therapy response. The outcome of patients within this subtype is, however, divergent. Some individuals show an increased risk of dying in the first five years, and others a long-term survival of over ten years after the diagnosis. In this study, we aim at identifying markers associated with basal-like patients’ survival and characterising subgroups with distinct disease outcome.MethodsWe explored the genomic and transcriptomic profiles of 351 basal-like samples from the METABRIC and ROCK data sets. Two selection methods, labelled Differential and Survival filters, were employed to determine genes/probes that are differentially expressed in tumour and control samples, and are associated with overall survival. These probes were further used to define molecular subgroups, which vary at the microRNA level and in DNA copy number.ResultsWe identified the expression signature of 80 probes that distinguishes between two basal-like subgroups with distinct clinical features and survival outcomes. Genes included in this list have been mainly linked to cancer immune response, epithelial-mesenchymal transition and cell cycle. In particular, high levels of CXCR6, HCST, C3AR1 and FPR3 were found in Basal I; whereas HJURP, RRP12 and DNMT3B appeared over-expressed in Basal II. These genes exhibited the highest betweenness centrality and node degree values and play a key role in the basal-like breast cancer differentiation. Further molecular analysis revealed 17 miRNAs correlated to the subgroups, including hsa-miR-342-5p, -150, -155, -200c and -17. Additionally, increased percentages of gains/amplifications were detected on chromosomes 1q, 3q, 8q, 10p and 17q, and losses/deletions on 4q, 5q, 8p and X, associated with reduced survival.ConclusionsThe proposed signature supports the existence of at least two subgroups of basal-like breast cancers with distinct disease outcome. The identification of patients at a low risk may impact the clinical decisions-making by reducing the prescription of high-dose chemotherapy and, consequently, avoiding adverse effects. The recognition of other aggressive features within this subtype may be also critical for improving individual care and for delineating more effective therapies for patients at high risk.Electronic supplementary materialThe online version of this article (doi:10.1186/s12920-017-0250-9) contains supplementary material, which is available to authorized users.

show abstract

“…An increasing number of lncRNAs have been identified as playing critical roles in cancer development and progression [43-45]. LncRNA H19 is located on the 11p15.5 locus and functions as an oncogene in several cancers [46-48]. Here, we initially analyzed lncRNA microarray profiles to identify candidate lncRNAs associated with the cytotoxic role of Huaier extract.…”

Section: Discussionmentioning

confidence: 99%

Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway

Wang

Chen

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Increasing evidence indicates that Huaier extract has promising therapeutic effects against cancer. However, the mechanisms that underlie its anti-tumor effects remain unclear. In recent years, various studies have shown that long noncoding RNAs (lncRNAs) play a critical role in the regulation of cancer development and progression. Here, we explored the role of lncRNAs in Huaier-induced tumor suppression. Methods: Microarray profiling was performed to identify the candidate lncRNAs affected by Huaier extract. Quantitative realtime PCR (qPCR) was used to evaluate the transfection efficiency and the influence of Huaier extract on H19 expression. The effect of Huaier extract on the cell viability was examined by MTT. Moreover, the rates of apoptotic cells were detected using flow-cytometric analysis. Western blot analysis was applied to show the protein levels of CBL. Results: Microarray data derived from Huaier-treated breast cancer cells identified H19 as a potential target. Huaier extract reduced the expression of H19. The over-expression of H19 inhibited the cytotoxic effects of Huaier extract; in contrast, reduced H19 expression enhanced the function of Huaier extract. MiR-675-5p was identified as a mature product of H19. Moreover, Huaier extract reduced the miR-675-5p expression. Upregulating miR-675-5p reversed the inhibitory effects of Huaier extract, whereas downregulating miR-675-5p sensitized breast cancer cells to the effect of Huaier extract. In addition, Huaier extract increased the expression of CBL protein, a direct target of miR-675-5p. Conclusion: Collectively, the data demonstrate that Huaier extract reduces viability and induces apoptosis in breast cancer cells via H19-miR-675-5p-CBL axis regulation.

show abstract

Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer

Cited by 109 publications

References 57 publications

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway

Basal-like breast cancer: molecular profiles, clinical features and survival outcomes

Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway

Contact Info

Product

Resources

About