Knockdown long noncoding RNA nuclear paraspeckle assembly transcript 1 suppresses colorectal cancer through modulating miR‐193a‐3p/KRAS

Zhu, Zhouting; Du, Shangce; Yin, Kai; Ai, Shichao; Yu, Mengchao; Liu, Yanqing; Shen, Yan; Liu, Minghui; Jiao, Rui‐Hua; Chen, Xi; Guan, Wenxian

doi:10.1002/cam4.1798

Cited by 25 publications

(31 citation statements)

References 62 publications

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“…Additionally, it has been reported that the regulation of miRNAs mediated by lncRNAs is involved in tumorigenesis and progression. For instance, the lncRNA nuclear paraspeckle assembly transcript 1 acts as a miR-193a-3p sponge to modulate the miR-193a-3p/KRAS pathway in colorectal cancer (17); lncRNA prostate cancer associated transcript-1 can promote NSCLC progression through competitively binding miR-149-5p and regulating the miR-149-5p/LRIG2 axis (18). In addition, lncATB serves as a molecular sponge to suppress interactions between miR-200b and Kindlin-2 in esophageal squamous cell carcinoma (19).…”

Section: Introductionmentioning

confidence: 99%

lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA‑101

Sun

Yang

et al. 2019

Mol Med Report

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MicroRNA (miR)-101 copy loss is an early event in the development of human lung cancer, and it occurs in 29% of all lung cancer incidences. In addition, miR-101 expression in non-small cell lung cancer (NSCLC) is known to be downregulated. The aim of the present study was to explore the roles and mechanisms of the long non-coding (lnc)-RNA pro-transition associated RNA (PTAR) on NSCLC cell proliferation, migration and invasion in association with miR-101. Reverse transcription-quantitative PCR analysis was performed to detect the expression of lncRNA PTAR in 30 paired human NSCLC tissues and the corresponding para-tumor tissues. PTAR was amplified and cloned into the expression vector pCDNA3.1. Then, PTAR-overexpression plasmids or small interfering (si)-RNA-PTAR was transfected into A549 cells for 48 h, after which cell proliferation and the cell cycle distribution were evaluated. In addition, Transwell chamber and cell scratch-wound assays were conducted to analyze A549 cell migration and invasion. A luciferase activity assay was evaluated to determine the interaction between PTAR and miR-101. Furthermore, our results demonstrated that in human NSCLC tissues and cell lines, lncRNA PTAR expression was upregulated compared with normal lung tissues and cell lines, respectively. Additionally, PTAR transfection was observed to promote A549 cell proliferation, migration and invasion; opposing effects were observed with siRNA-PTAR transfection. The luciferase activity assay revealed that PTAR could act as a sponge to bind miR-101. Thus, miR-101 plays a role in NSCLC tumorigenesis and progression. In conclusion, lncRNA PTAR was proposed to promote NSCLC cell growth through sponging and inactivating miR-101, which may be a possible mechanism underlying miR-101 copy loss in human NSCLC.

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Section: Introductionmentioning

confidence: 99%

lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA‑101

Sun

Yang

et al. 2019

Mol Med Report

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“…NOVA1, a member of the NOVA family of neuron-specific RNA-binding proteins, is aberrantly downregulated in multiple human cancers and affects a variety of pathophysiological processes associated with carcinogenesis and cancer progression (50)(51)(52). The expression and roles of NEAT1 and roles have been studied in other human cancers (43)(44)(45)(46)(47)(48)(49). Herein, we identified a novel NEAT1-miR-592-NOVA1 pathway, and this pathway could serve crucial roles in the aggressiveness of thyroid cancer.…”

Section: Discussionmentioning

confidence: 97%

“…In the present study, NOVA1 was validated as a direct target of miR-592 in thyroid cancer cells, and NEAT1 was proposed to function as a ceRNA to modulate NOVA1 expression by sponging miR-592. Multiple studies reported that NEAT1 is expressed at high levels and exerts oncogenic roles in a variety of human cancers, including cervical cancer (43), nasopharyngeal carcinoma (44), breast cancer (45), non-small cell lung cancer (46), colorectal cancer (47,48), and oral squamous cell carcinoma (49). NEAT1 is also upregulated in thyroid cancer (35)(36)(37), and upregulation of NEAT1 is positively correlated with TNM stage and tumor size (35).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-592 suppresses the malignant phenotypes of thyroid cancer by regulating lncRNA NEAT1 and downregulating NOVA1

et al. 2019

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Numerous studies have demonstrated that various microRNAs (miRs) are aberrantly expressed in thyroid cancer and play critical roles in thyroid cancer malignancy. The aberrant expression of miR-592 has frequently been reported in multiple human cancer types; however, its expression profile and functions in thyroid cancer remain poorly understood. Reverse transcription-quantitative polymerase chain reaction was carried out to determine the expression profile of miR-592 in thyroid cancer tissues and cell lines. The regulatory effects of miR-592 upregulation on thyroid cancer cell proliferation, migration, and invasion in vitro, and tumor growth in vivo were investigated using a ccK-8 assay, migration and invasion assays, and a xenograft tumor model, respectively. Furthermore, the mechanisms underlying miR-592-mediated suppression of the aggressive phenotypes of thyroid cancer cells were explored in detail. The results indicated that miR-592 was significantly downregulated in thyroid cancer samples, and its downregulation was associated with lymph node metastasis and tumor-node-metastasis stage. Patients with thyroid cancer and low miR-592 expression exhibited shorter overall survival than patients with high miR-592 expression. Overexpression of miR-592 resulted in decreased cell proliferation, migration, and invasion in thyroid cancer. In addition, neuro-oncological ventral antigen 1 (NOVA1) was identified as a novel target gene of miR-592 in thyroid cancer cells. Furthermore, ectopic NOVA1 expression may effectively abolish the tumor-suppressing effects of miR-592 overexpression in thyroid cancer cells. Notably, the lncRNA NEAT1 was proposed to function as a sponge of miR-592 in thyroid cancer cells, thereby regulating NOVA1 expression. Finally, resuming miR-592 expression significantly impaired thyroid cancer tumor growth in vivo. The results indicated that the NEAT1/miR-592/NOVA1 pathway may play regulatory roles in thyroid cancer malignancy in vitro and in vivo. Our findings may provide novel insight into the pathogenesis of thyroid cancer. Therefore, this pathway may be an effective target for treating patients with this disease.

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“…NEAT1 was identified as a sponge of miR‐193a‐3p. Zhu et al () pointed out that NEAT1 could target miR‐193a‐3p to regulate the proliferation, migration, and apoptosis of colorectal cancer in vitro and meditate tumor growth in vivo (Zhu et al, ). NEAT1 has been widely studied in many human malignancies.…”

Section: Discussionmentioning

confidence: 99%

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

Yang

et al. 2020

Cell Biology International

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Long non‐coding RNAs (lncRNAs) were reported to be involved in the progression of osteoarthritis (OA). The aim of this work was to explore the functional role of lncRNA nuclear‐enriched abundant transcript 1 (NEAT1) in OA. Reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of microRNA (miR‐193a)‐3p, NEAT1, and sex‐determining region Y‐box protein 5 (SOX5), as well as the levels of pro‐inflammatory cytokines interleukin‐6 (IL‐6), IL‐1β, tumor necrosis factor‐α (TNF‐α), and IL‐8 in OA cartilage tissue and chondrocytes. In addition, flow cytometry was used to measure the apoptosis of chondrocytes. The protein levels of extracellular matrix ACAN, collagen type II α1 chain (Col2a1), matrix metalloproteinase‐3 (MMP‐3), MMP‐13, a disintegrin, and metalloproteinase with thrombospondin motifs (ADAMTS)‐5 and SOX5 were determined using western blot analysis. Dual‐luciferase reporter assay was performed to determine the target relationship among NEAT1, miR‐193a‐3p, and SOX5. We found that miR‐193a‐3p expression was downregulated, while NEAT1 and SOX5 were upregulated in OA cartilage tissue and chondrocytes. Both upregulation of miR‐193a‐3p and knockdown of NEAT1 suppressed inflammation, apoptosis, and reduced the protein levels of MMP‐3, MMP‐13, and ADAMTS‐5, while elevating ACAN and Col2a1 expression in chondrocytes. NEAT1 targeted miR‐193a‐3p, and SOX5 was targeted by miR‐193a‐3p. Silencing of miR‐193a‐3p reversed the NEAT1 knockdown‐mediated effect on the inflammation, apoptosis, and production of the extracellular matrix. The introduction of SOX5 abolished the impact of the upregulation of miR‐193a‐3p on inflammation, apoptosis, and production of extracellular matrix in chondrocytes. In conclusion, NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human OA.

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Knockdown long noncoding RNA nuclear paraspeckle assembly transcript 1 suppresses colorectal cancer through modulating miR‐193a‐3p/KRAS

Cited by 25 publications

References 62 publications

lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA‑101

lncRNA PTAR promotes NSCLC cell proliferation, migration and invasion by sponging microRNA‑101

MicroRNA-592 suppresses the malignant phenotypes of thyroid cancer by regulating lncRNA NEAT1 and downregulating NOVA1

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

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