Long noncoding RNA SMAD5‐AS1 acts as a microRNA‐106a‐5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma

Zheng, Yanjun; Zhao, Jingyi; Liang, Tian; Wang, Ping; Wang, Juan; Yang, Daoke; Liu, Zhangsuo

doi:10.1096/fj.201900803r

Cited by 43 publications

(37 citation statements)

References 43 publications

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“…samples obtained from 68 patients. Functionally, differentially expressed lncRNAs are known as oncogenic factors in various human cancers 19,[33][34][35] In this study, we determined that LINC01106 exerted oncogenic role in CRC through promoting cell proliferation, mobility, EMT, and stemness. Our study is the first one to reveal the functions of LINC01106 in CRC progression.…”

Section: Discussionmentioning

confidence: 98%

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LINC01106 drives colorectal cancer growth and stemness through a positive feedback loop to regulate the Gli family factors

et al. 2020

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Long non-coding RNAs (lncRNAs) are essential contributors to the progression of various human cancers. Long intergenic non-protein coding RNA 1106 is a member of lncRNAs family. Until now, the specific role of LINC01106 in CRC remains undefined. The aim the current study was to unveil the functions of LINC01106 and explore its potential molecular mechanism in CRC. Based on the data of online database GEPIA, we determined that LINC01106 was expressed at a high level in colon adenocarcinoma (COAD) tissues compared to normal colon tissues. More importantly, high level of LINC01106 had negative correlation with the overall survival of COAD patients. Additionally, we also determined the low level of LINC01106 in normal colon tissues based on UCSC database. Through qRT-PCR, we identified that LINC01106 was highly expressed in CRC tissues compared to adjacent normal ones. Similarly, we detected the expression of LINC01106 and confirmed that LINC01106 was expressed higher in CRC cells than that in normal cells. Subsequently, LINC01106 was mainly distributed in the cytoplasm. LINC01106 induced the proliferation, migration, and stem-like phenotype of CRC cells. Mechanistically, cytoplasmic LINC01106 positively modulated Gli4 in CRC cells by serving as a miR-449b-5p sponge. Furthermore, nuclear LINC01106 could activate the transcription of Gli1 and Gli2 through recruiting FUS to Gli1 and Gli2 promoters. Mechanism of investigation unveiled that Gli2 was a transcription activator of LINC01106. In conclusion, Gli2-induced upregulation of LINC01106 aggravates CRC progression through upregulating Gli2, Gli2, and Gli4.

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Section: Discussionmentioning

confidence: 98%

“…Mechanistically, lncRNAs can regulate the expression of their downstream genes at transcriptional or posttranscriptional level. LncRNAs can act as positive regulators for mRNAs by acting as sponges for miRNAs [18][19][20][21] . In the current study, the possible downstream miRNAs of cytoplasmic LINC01106 were also detected.…”

Section: Introductionmentioning

confidence: 99%

LINC01106 drives colorectal cancer growth and stemness through a positive feedback loop to regulate the Gli family factors

et al. 2020

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“…Meanwhile, many studies have shown that one of the roles of lncRNAs is to regulate gene expression by competitively binding to miRNAs as competing endogenous RNAs (ceRNAs) in cancers. For instance, lncRNA linc00645 and SMAD5-AS1 have been reported as ceRNAs to mediate the progression of glioma and nasopharyngeal carcinoma by targeting miR-205-3p and miRNA-106a-5p, respectively (25,26). In the present study, we predicted miR-4722-3p as a potential downstream target of N13.3 by NONCODE database analysis.…”

Section: Discussionmentioning

confidence: 68%

Long non‑coding RNA RP11‑400N13.3 promotes the progression of colorectal cancer by regulating the miR‑4722‑3p/P2RY8 axis

Yang

Li²,

et al. 2020

Oncol Rep

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Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play significant roles in the development and progression of many types of cancer including colorectal cancer. RP11-400N13.3 is a novel lncRNA discovered recently and its biological function and underlying mechanism in colorectal cancer remain elusive. This study aimed to reveal the relationship between RP11-400N13.3 and colorectal cancer. Our results demonstrated that the expression of RP11-400N13.3 was significantly upregulated in both colorectal cancer tissues and cell lines as compared to normal adjacent tissues and normal colonic epithelial cells by RT-qPCR, respectively. Upregulation of RP11-400N13.3 was found to be correlated with a poor overall survival rate. Functional studies revealed that RP11-400N13.3 facilitated the proliferation, migration, invasion and tumor growth of colorectal cancer cells while inhibiting the apoptosis of cancer cells in vitro and in vivo. We also observed that RP11-400N13.3 serves as a sponge for miR-4722-3p, and that P2Y receptor family member 8 (P2RY8) was predicted to be a target of miR-4722-3p by bioinformatics analysis. Western blot assay indicated that the expression of P2RY8 was negatively or positively regulated by miR-4722-3p or RP11-400N13.3. In addition, rescue experiments revealed that RP11-400N13.3 promoted proliferation, migration and invasion by directly regulating the expression of miR-4722-3p and P2RY8. In conclusion, our results revealed that RP11-400N13.3 promoted colorectal cancer progression via modulating the miR-4722-3p/P2RY8 axis, thus suggesting RP11-400N13.3 as a potential therapeutic target for the treatment of colorectal cancer.

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“…More and more studies have shown that miRNAs play key roles in cancer chemotherapy resistance, and their potential role in determining drug sensitivity or drug resistance has been con rmed by several researches (14). As a member of the miR-17 family, miR-106a-5p is shown to be abnormally expressed in various tumors, including NPC (15), liver cancer (16) and colorectal cancer (17). Recently, overexpression of SOX4 has been found to be related to the occurrence, progression, invasion and metastasis in many various tumors, indicating that SOX4 may be a major determinant of NPC progression (18,19).…”

Section: Introductionmentioning

confidence: 96%

HOTAIR Promotes Cisplatin Resistance of Nasopharyngeal Carcinoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/SOX4 Axis

Cao

Sun

Liu

et al. 2020

Preprint

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Background: Nasopharyngeal carcinoma (NPC) is a highly malignant neoplasm originating from nasopharyngeal mucosa, and the emergence of multi-drug resistance poses a huge challenge for clinical treatment of NPC. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including NPC. However, the underlying mechanisms of HOTAIR involved in drug resistance in NPC are obscure.Methods: Quantitative polymerase chain reaction (qPCR) was employed to determine the HOTAIR, miR-106a-5p and SOX4 expression in NPC tissues and cells. The target relationship between HOTAIR and miR-106a-5p or miR-106a-5p and SOX4 was determined using dual-luciferase reporter assay. Cell proliferation, apoptosis, migration and invasion were explored using Cell counting kit-8 (CCK-8), flow cytometer and Transwell assays. The protein levels were confirmed using western blot.Results: Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant NPC tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance related gene expression, cell proliferation and invasion, and promoted apoptosis of C666-1/DDP and CNE2/DDP cells. Mechanism researches displayed that miR-106a-5p was down-regulated in DDP-resistant NPC tissues and cells. miR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. SOX4 was inhibited by miR-106a-5p at a posttranscriptional level, and the transfection of miR-106a-5p reversed the upregulation of SOX4 caused by HOTAIR overexpression. Increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion and apoptosis of C666-1/DDP and CNE2/DDP cells. Moreover, the transfection of SOX4 siRNA reversed the decrease of DDP resistance, cell proliferation and invasion, and rescued the increase of apoptosis induced by miR-106a-5p inhibition. Conclusions: These data suggested that HOTAIR enhanced DDP resistance of C666-1/DDP and CNE2/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/SOX4 axis.

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Long noncoding RNA SMAD5‐AS1 acts as a microRNA‐106a‐5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma

Cited by 43 publications

References 43 publications

LINC01106 drives colorectal cancer growth and stemness through a positive feedback loop to regulate the Gli family factors

LINC01106 drives colorectal cancer growth and stemness through a positive feedback loop to regulate the Gli family factors

Long non‑coding RNA RP11‑400N13.3 promotes the progression of colorectal cancer by regulating the miR‑4722‑3p/P2RY8 axis

HOTAIR Promotes Cisplatin Resistance of Nasopharyngeal Carcinoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/SOX4 Axis

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