Exploring the Secrets of Long Noncoding RNAs

Quan, Mingyang; Chen, Jinhui; Zhang, Deqiang

doi:10.3390/ijms16035467

Cited by 129 publications

(110 citation statements)

References 136 publications

(188 reference statements)

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“…Although many attributes of LncRNAs, such as patterns of expression, remain largely unknown, LncRNAs have been shown to play important roles in transcriptional, posttranscriptional, translational and epigenetic gene regulation [9,10]. An increasing amount of evidence has revealed that different LncRNAs might be associated with HCC [11].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Tan

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadherin, vimentin, Snail, Slug, Twist and Zeb1 in tissues and cells were determined by reverse transcription -quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. An MTT assay, scratch test and Transwell assay were applied to measure cell proliferation, migration and invasion, respectively. Results: The levels of JAK2, STAT3 and vimentin were higher in HCC tissues, while the expression of E-cadherin was lower in HCC tissues compared with para-cancerous tissues. The silencing of HOST2 significantly decreased cell proliferation, migration and invasion, reduced the levels of HOST2, JAK2, STAT3 and vimentin, and elevated the expression of E-cadherin. HOST2 silencing also decreased the levels of Snail, Slug and Twist but increased the level of Zeb1 protein, while the opposite findings were observed in the HOST2 mimic group. Conclusion: These results reveal a possible mechanism in HCC in which LncRNA HOST2 may increase EMT and enhance proliferation, invasion and metastasis of HCC cells via activation of the JAK2-STAT3 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway

Tan

Wang

et al. 2018

Cell Physiol Biochem

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“…Previous studies have demonstrated that abnormal expression of lncRNAs was able to change the biological functions of tumor cells by affecting various cellular processes. According to their alternative expression pattern, certain lncRNAs may reflect the progress of disease, and may be regarded as independent predictors for cancer diagnosis (14,16,31,32). The overexpression of Hox transcript antisense RNA in breast cancer promoted metastasis (33,34) and homeobox A transcript at the distal tip is considered an indicator for determining the progress of pancreatic cancer (35).…”

Section: Discussionmentioning

confidence: 99%

lncRNA C22orf32-1 contributes to the tumorigenesis of nasopharyngeal carcinoma

et al. 2017

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Abstract. The mechanism of nasopharyngeal carcinoma (NPC) remains unclear. The present study investigated the abnormal expression of long non-coding (lnc)RNAs in NPC tissues and one NPC cell line to identify the involvement of lncRNAs in the tumorigenesis of NPC. Using a quantitative reverse transcription polymerase chain reaction (RT-qPCR), the expression of lncRNA C22orf32-1 in NPC tissues and an NPC cell line was verified. The effects of lncRNA C22orf32-1 on NPC cells were investigated with a cell proliferation assay, cell scratch assay, Transwell assay and a cell apoptosis assay. The expression levels of lncRNA C22orf32-1 in NPC tissues and an NPC cell line were upregulated. lncRNA C22orf32-1 promoted the proliferation, migration and invasion of NPC cells, and reduced the apoptosis of NPC cells. The data demonstrated that lncRNA C22orf32-1 may facilitate the tumorigenesis of NPC, and may be used for the early diagnosis and treatment of NPC.

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“…gencodegenes.org/). Their functional role remains mostly elusive, however there are cases implicating lncRNAs in gene expression (at transcriptional, post-transcriptional and epigenetic level) and thus numerous cellular processes [3].…”

Section: Introduction Q4mentioning

confidence: 99%