H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT

Ma, Chao; Nong, Kate; Zhu, Hongda; Wang, Weiwei; Huang, Xinyu; Zhang, Yuan; Ai, Kaixing

doi:10.1007/s13277-014-2185-5

Cited by 254 publications

(177 citation statements)

References 42 publications

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“…H19 was characterized as an oncogenic lncRNA in some tumors and upregulated remarkably in primary PDAC tumors that subsequently metastasized, compared to those with non-metastasis. H19 also promoted PDAC cell invasion and migration at least partially by increasing HMGA2-mediated epithelial-mesenchymal transition (EMT) through antagonizing let-7 (53). The previous studies also reported several other lncRNAs related to PDAC, such as HULC, PVTI, MAP3K14, PPP3Cb, DAPKI and LOC285194 (54)(55)(56)(57).…”

Section: Discussionmentioning

confidence: 90%

Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma

Zhou

Gong

Jiang

et al. 2015

International Journal of Oncology

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Abstract. Long non-coding RNA (lncRNA) is a variety of the human transcriptome that does not code for proteins and plays an important role in the development and progression of multiple solid malignant tumors. However, the roles of lncRNAs in the development of pancreatic ductal adenocarcinoma (PDAC) remain unknown. In this study, we investigated the expression patterns of lncRNAs in three PDAC tumor samples (T) relative to those of matched adjacent non-tumor tissues (N) via a microarray with 30,586 lncRNA probes and 26,109 mRNA probes. The lncRNA microarray revealed 27,279 lncRNAs in PDAC samples, of which 2,331 were significantly upregulated (P<0.05; T/N>2.0) and 1,641 were downregulated (P<0.05; N/T>2.0) compared with matched adjacent non-tumor samples. In addition, 19,995 mRNAs were detected, of which 1,676 were significantly upregulated (P<0.05; T/N>2.0) and 1,981 were downregulated (P<0.05; N/T>2.0). Pathway analysis indicated that 41 pathways corresponded to upregulated transcripts and 25 pathways corresponded to downregulated transcripts (P-value cut-off is 0.05). Gene ontology (GO) analysis showed that the highest enriched GOs targeted by upregulated and downregulated transcripts were tissue homeostasis. The validation results from quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis and microarray analysis were consistent. Furthermore, the expression level of long intergenic non-coding RNA HOTAIRM1 was upregulated in 12 PDAC tissues samples compared with matched adjacent non-tumor samples by qRT-PCR. The results showed that the lncRNA and mRNA expression profiles differed significantly between the PDAC tissues and their adjacent non-tumor tissues, and the revelation of an association between HOTAIRM1 expression and PDAC is especially noteworthy. These findings may provide new potential molecular markers for diagnosis and treatment of PDAC.

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Section: Discussionmentioning

confidence: 90%

Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma

Zhou

Gong

Jiang

et al. 2015

International Journal of Oncology

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“…Previous researches highlighted the post-transcriptional repression of HMGA2 by several miRNAs, such as let-7 29 , miR-33a 30 and miR-204 31 . Gong et al found that lncRNA H19 promoted HMGA2-mediated epithelial-mesenchymal transition through antagonizing let-7 32 . Study of Deng et al also showed that a lncRNA, CCAT1 functions as a molecular sponge for let-7 and leads to the derepression of its endogenous targets HMGA2 33 .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HIT000218960 promotes papillary thyroid cancer oncogenesis and tumor progression by upregulating the expression of high mobility group AT-hook 2 (HMGA2) gene

Yang

et al. 2016

Cell Cycle

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Accumulating evidence suggests that long noncoding RNAs (lncRNAs) play an important role in oncogenesis and tumor progression. However, our knowledge of lncRNAs in thyroid cancer is still limited. To explore the crucial lncRNAs involved in oncogenesis of papillary thyroid cancer (PTC), we acquired data of differentially expressed lncRNAs between PTC tissues and paired adjacent noncancerous thyroid tissues through lncRNA microarray. In the microarray data, we observed that a newly identified lncRNA, HIT000218960, was significantly upregulated in PTC tissues and associated with a well-known oncogene, high mobility group AT-hook 2 (HMGA2) gene. Both in normal thyroid tissues and PTC tissues, the expression of HIT000218960 was significantly positively correlated with that of HMGA2 mRNA. Knockdown of HIT000218960 in PTC cells resulted in downregulation of HMGA2. In addition, functional assays indicated that inhibition of HIT000218960 in PTC cells suppressed cell proliferation, colony formation, migration and invasion in vitro. Increased HIT000218960 expression in PTC tissues was obviously correlated with lymph node metastasis and multifocality, as well as TNM stage. Those findings suggest that HIT000218960 might acts as a tumor promoter through regulating the expression of HMGA2.

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“…H19 promotes EMT via antagonizing let-7 and contributing to HMGA2-mediated EMT in pancreatic ductal adenocarcinoma (17), or by being associated with enhancer of zeste homolog 2 (EZH2) and activating wingless/β-catenin to decrease E-cadherin in bladder cancer (34). H19 has been identified to encode microRNA-675 (miR-675), and a positive feedback loop between H19/miR-675 and Slug has been reported to attenuate E-cadherin and lead to EMT in certain cancer cell lines (16).…”

Section: Discussionmentioning

confidence: 99%

“…H19 is initially suggested as a suppressor for tumor development and metastasis (12,13). However, previously H19 has been proposed as an oncogenic lncRNA in numerous cancers (14,15), and is found to positively regulate the metastatic potential of cancer cells (16,17). In endometrioid endometrial cancer tissues (18)(19)(20), overexpression of H19 exists and is associated with neoplastic cell invasion.…”

Section: Introductionmentioning

confidence: 99%

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H19 promotes endometrial cancer progression by modulating epithelial-mesenchymal transition

Zhao

Chen

et al. 2016

Oncology Letters

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Abstract. Endometrial cancer is one of the most common types of gynecological malignancy worldwide. Novel biomarkers and therapeutic targets are imperative for improving patients' survival. Previous studies have suggested the long non-coding RNA H19 as a potential cancer biomarker. To investigate the role of H19 in endometrial cancer, the present study examined the expression pattern of H19 in endometrial cancer tissues by quantitative polymerase chain reaction, and characterized its function in the endometrial cancer cell line via knocking down its expression with small interfering RNAs. It was found that H19 level was significantly higher in tumor tissues than in paratumoral tissues. Knockdown of H19 did not affect the growth rate of HEC-1-B endometrial cancer cells, but significantly suppressed in vitro migration and invasion of HEC-1-B cells. Furthermore, H19 downregulation decreased Snail level and increased E-cadherin expression without affecting vimentin level, indicating partial reversion of epithelial-mesenchymal transition (EMT). The present findings suggested that H19 contributed to the aggressiveness of endometrial cancer by modulating EMT process.

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H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT

Cited by 254 publications

References 42 publications

Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma

Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma

Long noncoding RNA HIT000218960 promotes papillary thyroid cancer oncogenesis and tumor progression by upregulating the expression of high mobility group AT-hook 2 (HMGA2) gene

H19 promotes endometrial cancer progression by modulating epithelial-mesenchymal transition

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