LncRNA MCM3AP-AS1 serves as a competing endogenous RNA of miR-218 to upregulate GLUT1 in papillary thyroid carcinoma

Nian, Rui; Li, Wanjun; Li, Xiang; Zhang, Jiayu; Li, Weihua; Pan, Fanfan; Cheng, Jing; Jin, Xin

doi:10.20945/2359-3997000000510

Cited by 4 publications

(1 citation statement)

References 21 publications

(27 reference statements)

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“…MCM3AP-AS1 functions as an oncogene in many human cancers. For instance, high MCM3AP-AS1 expression was associated with hepatocellular carcinoma, thyroid cancer and endometrioid carcinoma cells' proliferation [8][9][10] . However, the underlying mechanism of MCM3AP-AS1 remains unexplored in OC cells.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA MCM3AP-AS1 promotes ovarian cancer cells progression by modulating miR-383/DDIT4 axis

Yan,

Chen,

Guo

2023

Preprint

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Long non-coding RNA (lncRNA) was recently reported to be implicated in cancer progression. However, the role of MCM3AP-AS1 in ovarian cancer (OC) remains undetected. In this study, MCM3AP-AS1 expression was elevated in OC tissues. High MCM3AP-AS1 expression was related to advanced tumor stage and poor survival. MCM3AP-AS1 knockdown inhibited OC cells proliferation, migration, invasion and EMT in vitro and suppressed primary tumor growth in vivo. Mechanically, MCM3AP-AS1 sponged miR-383 and upregulated the expression of DDIT4. In addition, the suppression of EMT induced by silencing of MCM3AP-AS1 involved with miR-383 inhibition. In sum, MCM3AP-AS1 promoted cell progression through regulating miR-383/DDIT4, which suggested a novel potential oncogenic target for OC.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA MCM3AP-AS1 promotes ovarian cancer cells progression by modulating miR-383/DDIT4 axis

Yan,

Chen,

Guo

2023

Preprint

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Biological and therapeutic viewpoints towards role of miR-218 in human cancers: Revisiting molecular interactions and future clinical translations

Hashemi

Gholami

Raesi

et al. 2023

Cellular Signalling

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LINC00887 Acts as an Enhancer RNA to Promote Medullary Thyroid Carcinoma Progression by Binding with FOXQ1

Liu,

Wang,

et al. 2024

CCDT

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Background:: Medullary thyroid carcinoma (MTC) is a rare but aggressive endocrine malignancy that originates from the parafollicular C cells of the thyroid gland. Enhancer RNAs (eRNAs) are non-coding RNAs transcribed from enhancer regions, which are critical regulators of tumorigenesis. However, the roles and regulatory mechanisms of eRNAs in MTC remain poorly understood. This study aims to identify key eRNAs regulating the malignant phenotype of MTC and to uncover transcription factors involved in the regulation of key eRNAs. Methods:: GSE32662 and GSE114068 were used for the identification of differentially expressed genes, eRNAs, enhancers and enhancer-regulated genes in MTC. Metascape and the transcription factor affinity prediction method were used for gene function enrichment and transcription factor prediction, respectively. qRT-PCR was used to detect gene transcription levels. ChIP-qPCR was used to assess the binding of histone H3 lysine 27 acetylation (H3K27ac)-enriched regions to anti- H3K27ac. RIP-qPCR was used to detect the binding between FOXQ1 and LINC00887. CCK8 and Transwell were performed to measure the proliferation and invasion of MTC cells, respectively. Intracellular reactive oxygen species (ROS) levels were quantified using a ROS assay kit. Results:: Four eRNAs (H1FX-AS1, LINC00887, MCM3AP-AS1 and A1BG-AS1) were screened, among which LINC00887 was the key eRNA promoting the proliferation and invasion of MTC cells. A total of 135 genes controlled by LINC00887-regulated enhancers were identified; among them, BCL2, PRDX1, SFTPD, TPO, GSS, RAD52, ZNF580, and ZFP36L1 were significantly enriched in the “ROS metabolic process” term. As a transcription factor regulating genes enriched in the “ROS metabolic process” term, FOXQ1 could recruit LINC00887. Overexpression of FOXQ1 restored LINC00887 knockdown-induced downregulation of GSS and ZFP36L1 transcription in MTC cells. Additionally, FOXQ1 overexpression counteracted the inhibitory effects of LINC00887 knockdown on the proliferation and invasion of MTC cells and the promotion of intracellular ROS accumulation induced by LINC00887 knockdown. Conclusion:: LINC00887 was identified as a key eRNA promoting the malignant phenotype of MTC cells. The involvement of FOXQ1 was essential for LINC00887 to play a pro-tumorigenic role in MTC. Our findings suggest that the FOXQ1/LINC00887 axis is a potential therapeutic target for MTC.

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LncRNA MCM3AP-AS1 serves as a competing endogenous RNA of miR-218 to upregulate GLUT1 in papillary thyroid carcinoma

Cited by 4 publications

References 21 publications

Long noncoding RNA MCM3AP-AS1 promotes ovarian cancer cells progression by modulating miR-383/DDIT4 axis

Long noncoding RNA MCM3AP-AS1 promotes ovarian cancer cells progression by modulating miR-383/DDIT4 axis

Biological and therapeutic viewpoints towards role of miR-218 in human cancers: Revisiting molecular interactions and future clinical translations

LINC00887 Acts as an Enhancer RNA to Promote Medullary Thyroid Carcinoma Progression by Binding with FOXQ1

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