Long noncoding RNA ABHD11-AS1 functions as a competing endogenous RNA to regulate papillary thyroid cancer progression by miR-199a-5p/SLC1A5 axis

Xi, Zhaodong; Tong, Houchao; Ding, Yu; Wu, Luyao; Cai, Jing-Sheng; Si, Yan; Zhang, Hao; Shen, Mingqiang

doi:10.1038/s41419-019-1850-4

Cited by 65 publications

(62 citation statements)

References 36 publications

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“…Long non-coding RNA (LncRNA) FYVE, RhoGEF and PH domain containing 5 antisense RNA 1 (FGD5-AS1) has been reported as oncogene in colorectal cancer, promoting its tumorigenesis [16]. Mechanistically, lncRNAs can exert functions in human cancers by sequestering miRNAs to up-regulate downstream protein-coding mRNAs [17][18][19]. According to previous study, we can speculate that FGD5-AS1 has its critical role in tumor progression, and we found that it can sponge to miR-107 in our assays.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Fan

Li²,

et al. 2020

Bioscience Reports

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Long non-coding RNA (lncRNA) FYVE, RhoGEF and PH domain containing 5 antisense RNA 1 (FGD5-AS1) has been reported as an oncogene in colorectal cancer, promoting its tumorgenesis. The present paper focused on searching the potential function of FGD5-AS1 in non-small cell lung carcinoma (NSCLC). There are connections between the expression of lncRNA FGD5-AS1 and human NSCLC tumor growth and progression. Also, the relationships between FGD5-AS1, hsa-miR-107 and mRNA fibroblast growth factor receptor like 1 (FGFRL1) are going to test their interaction in NSCLC cell lines, which may cause a series of biological behaviors of NSCLC cells. qRT-PCR analysis was conducted to test the expression of RNAs in different situation. CCK-8 experiment and clone formation assay were performed to assess proliferation of NSCLC cells. Also, connection between FGD5-AS1 and hsa-miR-107 were investigated by luciferase reporter assay and RNA pull-down assay. Rescue experiments were performed to verify the modulating relationship between FGD5-AS1, hsa-miR-107 and FGFRL1. High-level expression of FGD5-AS1 was found in NSCLC. FGD5-AS1 may promote the proliferation of NSCLC cells. Also, the combination between hsa-miR-107, FGD5-AS1 and NSCLC have been proved, which means they can play an interaction function in NSCLC cells. Thence, we concluded that lncRNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Fan

Li²,

et al. 2020

Bioscience Reports

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“…Histological types of TC include papillary carcinoma (PTC), follicular carcinoma (FTC), anaplastic carcinoma (ATC)/undifferentiated carcinoma, and medullary carcinoma (MTC) [4], and there have been different mutational profiles in these subtypes. Recent studies have confirmed a few molecular markers that have allowed better understanding of the molecular mechanisms of TC, for instance, BRAF and RAS point mutations, RET/PTC and PAX8/PPAR gene rearrangements, and so on [5][6][7]. Targeting certain molecules associated with initiation and progression of TC will be a significant and promising research area.…”

Section: Introductionmentioning

confidence: 95%

Immunohistochemical Basigin Expression Level in Thyroid Cancer Tissues

Guo

Tang

Pang

et al. 2020

Preprint

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Background Thyroid cancer (TC) is the most common endocrine malignancy, Basigin (also known as BSG) plays a crucial role in tumor cell invasion, metastasis, and angiogenesis. This study was designed to identify the change of BSG expression in TC and its possible potential mechanism. Methods The BSG expression levels in TC were demonstrated using data collected from in-house immunohistochemical (IHC), RNA-sequencing (RNA-seq), microarrays and literatures. Integrated analysis was performed to determined BSG expression levels in TC comprehensively. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed with the integration of BSG co-expressed genes and differentially expressed genes (DEGs) in TC tissues to explore the potential mechanisms of BSG in TC. Results The protein expression level of BSG was significantly higher in TC cases based on the IHC experiments. In addition, the combined SMD for BSG expression was 0.39 (p < 0.0001), the diagnostic odds ratio was 3.69, and the AUC of the sROC curve was 0.6986 using 1182 TC cases and 437 non-cancerous cases from 17 independent datasets. Furthermore, BSG co-expressed genes tended to be enriched in gene terms of the extracellular matrix (ECM), cell adhesion, and cell-cell interactions. The expression levels of nine hub BSG co-expressed genes were markedly up-regulated in TC cases. Conclusion BSG expression levels were closely correlated with the progression of TC and may affect the signals of the ECM, cell adhesion, and cell-cell interactions.

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“…Recently, the incidence of thyroid cancer is ascending, which may be attributed to the improvement of the early diagnosis of thyroid cancer [4]. Although the therapeutic strategies, including thyroidectomy, radioiodine therapy and thyroid-stimulating hormone inhibition therapy, have greatly improved the survival quality of early thyroid cancer patients, the prognosis of advanced and metastatic patients is dissatisfactory [5]. Therefore, it is very meaningful to investigate the underlying molecular mechanism for providing the meritorious therapeutic protocol of thyroid cancer patients.…”

Section: Introductionmentioning

confidence: 99%

miR-154-3p and miR-487-3p synergistically modulate RHOA signaling in the carcinogenesis of thyroid cancer

et al. 2020

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Correspondence: Ning An (anning gpch@tom.com) Background: miRs family members are often thought to have extensively overlapping targets and synergistically to modulate target gene expression via post-transcriptional repression. The present study was to determine whether miR-154-3p and miR-487-3p synergistically collaborated to regulate RHOA signaling in the carcinogenesis of thyroid cancer. Materials and methods: Candidate miRs were filtrated using miR microarray assays. Gene and protein expression levels were analyzed using RT-qPCR and Western blotting, respectively. Cell growth was evaluated using CCK8 assays and nude-mouse transplanted tumor experiments. Cell apoptosis was detected using Annexin V-FITC double staining. Results: miR-154-3p and miR-487-3p were significantly decreased in 63 thyroid cancer tissues and cell lines compared with those in paired non-tumor tissues and normal thyroid follicular epithelial cells. Low expression levels of miR-154-3p and miR-487-3p significantly correlated with tumor size, TNM stage, histological grade, lymph node metastasis and shorter overall survival in patients with thyroid cancer. Furthermore, the protein expression of RHOA was significantly inversely correlated with miR-154-3p (r = −0.404; P = 0.001) and miR-487-3p (r = −0.456; P < 0.001) expression in thyroid cancer tissues. We experimentally validated that miR-154-3p and miR-487-3p synergistically blocked thyroid cancer cell growth in vitro and in vivo. However, the anti-proliferative and pro-apoptotic activities of miR-154-3p/487-3p were neutralized by RHOA overexpressed vectors. Conclusions: Our present findings expounded a novel signal cascade employing miR-154-3p/487-3p and RHOA to fine-tune thyroid cancer cell proliferation and apoptosis. We corroborated that suppression of RHOA by miR-154-3p/487-3p may be a valuable therapeutic target for impeding thyroid cancer progression.Ras homolog family member A (RHOA) as a representative protein of RHO subfamily primarily participates in actin cytoskeleton rearrangement, which is implicated in various physiological functions, including cell proliferation, differentiation, migration, polarity and gene transcription [6]. Rho-associated protein kinase (ROCK) is a downstream effector of RHOA and has the ability to modulate cytoskeleton dynamics [6]. Over-activation of RHOA/ROCK signaling pathway may be associated with a decrease in cell-cell junctions and a promotion of cell motility [7]. Previous studies have validated that high expression of RHOA and ROCK is frequently reported in various cancer-types, such as breast cancer, ovarian cancer and colon cancer [6,8,9]. In thyroid cancer, RHOA/ROCK signaling has a profound stimulative impact to facilitate the invasiveness of anaplastic thyroid cancer cells [10]. microRNAs (miRs) are a class of non-coding RNAs and have widely been elaborated in the pathogenesis of various diseases, including carcinogenesis [11]. miRs function as post-transcriptional regulators to repress target genes translation via binding with their 3 -un...

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Long noncoding RNA ABHD11-AS1 functions as a competing endogenous RNA to regulate papillary thyroid cancer progression by miR-199a-5p/SLC1A5 axis

Cited by 65 publications

References 36 publications

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Long non-coding RNA FGD5-AS1 promotes non-small cell lung cancer cell proliferation through sponging hsa-miR-107 to up-regulate FGFRL1

Immunohistochemical Basigin Expression Level in Thyroid Cancer Tissues

miR-154-3p and miR-487-3p synergistically modulate RHOA signaling in the carcinogenesis of thyroid cancer

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