LncRNA CASC2 expression is down- regulated in papillary thyroid cancer and promotes cell invasion by affecting EMT pathway

Zhou, Tao; Zhong, Meijun; Zhang, Shuyong; Wang, Zhi; Xie, Rong; Cai, Xiong; Lv, Yunxia; Chen, Wanzhi; Yu, Jichun

doi:10.3233/cbm-181198

Cited by 30 publications

(21 citation statements)

References 17 publications

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“…In this study, we found that CASC2 was lowly expressed in PTC tissues and cells and indicated poor prognosis of patients, which is also in agreement with former efforts [ 14 , 15 , 18 ]. 131 I therapy is a common strategy for the treatment of thyroid cancer.…”

Section: Discussionsupporting

confidence: 92%

“…Long noncoding RNA cancer susceptibility candidate 2 (CASC2) has been demonstrated as a tumor suppressor by regulating cell proliferation, apoptosis, migration, and chemoresistance in human cancers, including hepatocellular carcinoma, gastric cancer, and prostate cancer [ 11 – 13 ]. Furthermore, emerging evidences suggest that CASC2 is lowly expressed and inhibits cell proliferation in PTC [ 14 , 15 ]. However, little is known about the role of CASC2 in 131 I sensitivity to PTC.…”

Section: Introductionmentioning

confidence: 99%

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lncRNA CASC2 Enhances 131I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

Tao

Tian

et al. 2020

BioMed Research International

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Long noncoding RNA cancer susceptibility candidate 2 (CASC2) has been reported to play an anticancer role in papillary thyroid cancer (PTC). Radioiodine (131I) is a common option for the treatment of PTC. However, the role and mechanism of CASC2 in 131I sensitivity remain unclear. In this study, 131I-resistant cells were constructed through continuous treatment of 131I. The expression levels of CASC2 and miR-155 were measured by qRT-PCR. The IC50 of 131I was analyzed by cell viability using MTT assay. Flow cytometry was conducted to determine cell apoptosis induced by 131I. The association between CASC2 and miR-155 was evaluated by luciferase assay and RNA immunoprecipitation. A mouse xenograft model was built to explore the effect of CASC2 on the growth of 131I-resistant PTC cells in vivo. Results showed that CASC2 expression was decreased in PTC tissues and cells, and low expression of CASC2 was associated with poor outcome of patients. CASC2 level was reduced in 131I-resistant cells. Knockdown of CASC2 inhibited 131I sensitivity in thyroid cancer cells. Overexpression of CASC2 enhanced 131I sensitivity in constructed resistant PTC cells. CASC2 was a decoy of miR-155, and CASC2-mediated promotion of 131I sensitivity was weakened by decreasing miR-155. Abundance of CASC2 inhibited the growth of 131I-resistant cells in vivo. As a conclusion, CASC2 increases 131I sensitivity in PTC by sponging miR-155, providing a novel target for the treatment of thyroid cancer patients with 131I resistance.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

lncRNA CASC2 Enhances 131I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

Tao

Tian

et al. 2020

BioMed Research International

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“…LncRNAs can affect the stability of coding genes by regulating the activity of miRNAs, thereby regulating a variety of biological activities of tumor cells, including transcriptional regulation, post-transcriptional regulation, and phenotypic regulation (15).In previous studies, Zhou et al found that the expression of lncRNA CASC2 was associated with lymph node metastasis in PTC patients, which inhibited the proliferation, apoptosis and migration of cells (16).Also, Song et al con rmed that lncRNA ENST0000053963 could act as an oncogenic factor in PTC through MAPK signaling (17), suggesting that lncRNAs could function both as tumor suppressors and tumor promoters. In this study, according to the TCGA we newly discovered many lncRNAs aberrantly expressed in PTC tissues, of which Linc00460 may promote the invasion and metastasis of cancer, Linc00460 has been con rmed to be closely related to the progression of various cancers, such as its promotion of cell migration and invasion by regulating hnRNPK and induction of epithelial-mesenchymal transition in cell lung cancer.…”

Section: Discussionmentioning

confidence: 99%

lncRNA-miRNA-mRNA ceRNA Network in Thyroid Carcinoma from The Cancer Genome Atlas

Mo¹,

Jiang²,

Wang³

et al. 2020

Preprint

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Increasing evidence indicates that the competitive endogenous RNA (ceRNA) hypothesis, that is, long non-coding RNA (LncRNA) can competitively bind microRNA (miRNA) through miRNA response elements to affect the expression of target RNA, and dysregulation of LncRNA expression plays a key role in tumor progression. The papillary thyroid carcinoma that we studied is the most significant pathological type of thyroid cancer, but its ceRNA network has not been extensively evaluated. We analyzed level-3 data from RNA-Seq of 58 para-carcinoma tissues and 501 patients with primary papillary thyroid carcinoma (PTC) using the DEseq software package and downloaded clinical information from The Cancer Genome Atlas (TCGA) to find potential biomarkers or therapeutic targets. As a result, 149 differential miRNAs were selected, including 117 up -regulated, 32 down-regulated, and 3099 differential mRNAs, including 1976 up-regulated, 1123 down-regulated, and 434 differential lncRNAs, including 331 up-regulated and 103 down-regulated (Fold Change > 2, P < 0.05). The interactions between these differentially expressed RNA groups constitute the ceRNA network of PTC. Moreover, we used the microde database to predict the miRNAs that may be acted by the above screened differential lncRNAs and intersected with the selected miRNAs, and further predicted the target genes of the intersecting miRNAs by TargetScan, miRTarBase and miRDB, and intersected with the selected mRNAs. From the constructed ceRNA network we can see that Linc00460 may cause the invasion and metastasis of PTC by competitively inhibiting hsa-mir-150 and upregulating the expression of its downstream target gene EREG. Our study identified a series of lncRNAs associated with PTC progression and prognosis, and this complex ceRNA interaction network provides guidance for better understanding of the molecular mechanisms of PTC and can be used as an effective diagnostic tool for PTC invasion, metastasis and prognosis. Kaplan-Meier analysis of the differentially expressed RNAs associated with PTC pathogenesis confirmed that the lncRNAs AC097717.1, C20orf203, EMX2OS were potentially associated with the prognosis of PTC (P<0.05).

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“…Long non‐coding RNA (lncRNA) dysfunction is related to a wide range of diseases, such as cancer, neurodegeneration, cardiovascular disease and neurasthenia . For example, overexpressed lncRNA NR_036575.1 would lead to the proliferation and migration of papillary TC . In order to discover the genes that might be correlated with TC, the Gene Expression Omnibus (GEO) database was employed to retrieve the lncRNA trinucleotide repeat containing 6C (TNRC6C)‐AS1 was overexpressed in TC cells.…”

Section: Introductionmentioning

confidence: 99%

“…6 For example, overexpressed lncRNA NR_036575.1 would lead to the proliferation and migration of papillary TC. 7 In order to discover the genes that might be correlated with TC, the Gene Expression Omnibus (GEO) database was employed to retrieve the lncRNA trinucleotide repeat containing 6C (TNRC6C)-AS1 was overexpressed in TC cells. Therefore, lncRNA TNRC6C-AS1 was the main focus of our study.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

Peng

Tan

et al. 2019

J Cellular Molecular Medi

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The role of long non‐coding RNAs (lncRNAs) in thyroid carcinoma (TC), the most frequent endocrine malignancy, has been extensively examined. This study investigated effect of interaction among lncRNA TNRC6C‐AS1, serine/threonine‐protein kinase 4 (STK4) and Hippo signalling pathway on TC. Initially, lncRNA TNRC6C‐AS1 expression in TC tissues was detected. To explore roles of lncRNA TNRC6C‐AS1, STK4 and Hippo signalling pathway in TC progression, their expressions were altered. Interaction between lncRNA TNRC6C‐AS1 and STK4, STK4 promoter methylation, or Hippo signalling pathway was verified. After that, a series of experiments were employed to evaluate in vitro ability of apoptosis, proliferation and autophagy of TC cells and in vivo tumorigenicity, and tumour growth of TC cells. lncRNA TNRC6C‐AS1 was highly expressed while STK4 was poorly expressed in TC tissues. LncRNA TNRC6C‐AS1 promoted the STK4 methylation and down‐regulated STK4 expression, which further activated the Hippo signalling pathway. STK4 silencing was observed to promote the proliferation ability of TC cells, inhibit the apoptosis and autophagy abilities, as well as enhance the tumorigenicity and tumour growth. Moreover, the in vitro proliferation ability as well as the in vivo tumorigenicity and tumour growth of TC cells were inhibited after the blockade of Hippo signalling pathway, while the apoptosis and autophagy abilities were promoted. The results demonstrate that the lncRNA TNRC6C‐AS1 increases STK4 promoter methylation to down‐regulate STK4 expression, thereby promoting the development of TC through activation of Hippo signalling pathway. It highlights that lncRNA TNRC6C‐AS1 may be a novel therapeutic target for the treatment of TC.

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LncRNA CASC2 expression is down- regulated in papillary thyroid cancer and promotes cell invasion by affecting EMT pathway

Abstract: Thus, these results indicated that lncRNA CASC2 was a predictor for LNM of PTC patients and may serve as a potential target of PTC treatment.

Cited by 30 publications

References 17 publications

lncRNA CASC2 Enhances 131I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

lncRNA CASC2 Enhances 131I Sensitivity in Papillary Thyroid Cancer by Sponging miR-155

lncRNA-miRNA-mRNA ceRNA Network in Thyroid Carcinoma from The Cancer Genome Atlas

Long non‐coding RNA TNRC6C‐AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway

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