lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial‐mesenchymal transition in bladder cancer

Qiu, Feng; Zhang, Ming‐ran; Zhou, Zhen; Pu, Jinxian; Zhao, Xiaojun

doi:10.1002/jcb.28373

Cited by 32 publications

(27 citation statements)

References 25 publications

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“…In bladder cancer, miR503HG was also downregulated and suppressed cancer progression by inhibiting cancer cell proliferation and invasion. 17 Similarly, we also Figure 2 Cisplatin treatment further downregulated miR503HG in both patients and CSCC cells. Expression levels of miR503HG in plasma collected from CSCC patients at 0, 3, 6 and 9 weeks after the initiation of cisplatin treatment were measured by qPCR.…”

Section: Discussionsupporting

confidence: 62%

“…15 LncRNA MIR503 Host Gene (miR503HG) has been reported to be a tumor suppressor in several types of cancers. 16,17 However, its exact functioning role in cervical cancer is unclear. By analyzing the TCGA dataset, we found that miR503HG was significantly downregulated in cervical squamous cell carcinoma (CSCC), which is a major subtype of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

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<p>LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3</p>

Zhao¹,

Yu²,

Wang³

2020

CMAR

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Introduction: The purpose of this study is to investigate the role of long non-coding RNA (lncRNA) miR503 Host Gene (miR503HG) in cervical squamous cell carcinoma (CSCC). Methods: Analysis of TCGA dataset revealed that expression levels of miR503HG in CSCC tissues were over 12 times lower than those in non-tumor tissues, indicating its involvement in CSCC. Results: In this study, we observed that levels of miR503HG in plasma were significantly lower in CSCC patients than in healthy participants. The cisplatin-based treatment further downregulated miR503HG in both patients and CSCC cells. MiR503HG overexpression in CSCC cells led to the suppression of miR-155 and elevation of Caspase-3, acting as the downstream target of miR-155. Cell apoptosis analysis showed that miR503HG and Caspase-3 overexpression led to an increased cell apoptosis rate under Cisplatin treatment. MiR-155 played the opposite role and attenuated the functions of Caspase-3 and miR503HG overexpression. Conclusion: Therefore, miR503HG may regulate the drug resistance of CSCC cells by regulating mir-155/Caspase-3.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

<p>LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3</p>

Zhao¹,

Yu²,

Wang³

2020

CMAR

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“…LncRNA PEG10 interacted with miR‐29b to enhance BC cell proliferation, migration and invasion . In addition, Qiu et al demonstrated that lncRNA MIR503HG acted as a tumor suppressor, which inhibited cell proliferation, metastasis and epithelial‐mesenchymal transition process in BC . It was described that MBNL1‐AS1 was a novel lncRNA to potentially predict the prognosis of gastric cancer .…”

Section: Discussionmentioning

confidence: 99%

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

et al. 2019

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LncRNAs have been shown to play essential roles in bladder cancer (BC) progress.Our microarrays of clinical samples firstly screened that lncRNA muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) was poorly expressed in BC tissues. However, its biological function in BC remains not well understood. Here we examined the clinical correlations with MBNL1-AS1 in BC patients. Then, 5673 and T24 cell lines were employed to investigate the role of MBNL1-AS1 in the proliferation and apoptosis of BC cells in vitro and in vivo. Furthermore, miR-135a-5p (miR-135a)/PHLPP2/FOXO1 axis was focused to explore its regulatory mechanism in BC.The results showed that MBNL1-AS1 was significantly downregulated in bladder tumor tissues, and associated with BC progression. In vitro, MBNL1-AS1 knockdown increased the number of viable cells and bromodeoxyuridine-positive cells, accelerated cell cycle, and dysregulated proliferative regulators (Ki67, p21, p27, and Cyclin D1) in BC cells. The apoptotic cells and the cleavages of caspase-3/9 were reduced in MBNL1-AS1-silenced BC cells. Overexpression of MBNL1-AS1 had opposite effects on BC cell proliferation and apoptosis. Moreover miR-135a was demonstrated to interact with MBNL1-AS1, and inhibiting miR-135a reversed the effects of shMBNL1-AS1 on BC cells. The downstream effectors (PHLPP2 and FOXO1) were positively regulated by MBNL1-AS1, but negatively regulated by miR-135a. Similar results were also observed in xenograft tumors. In conclusion, this study firstly suggests that MBNL1-AS1 acts as a tumor suppressor of BC by targeting miR-135a/PHLPP2/FOXO1 axis, providing a novel insight for BC diagnosis and treatment. K E Y W O R D S bladder cancer, FOXO1, MBNL1-AS1, miR-135a-5p, PHLPP2 | 725 WEI Et al.

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“…Qiu et al suggested that MIR503HG exhibited significant antiproliferation, antimigration/invasion effects on bladder cancer cells [31]. Chou et al demonstrated that MIR503HG overexpression inhibits colorectal cancer (CRC) cell migration and invasion mediated by TGF-β2 [32].…”

Section: Accepted Articlementioning

confidence: 99%

Identification of crucial noncoding RNAs and mRNAs in hypertrophic scars via RNA sequencing

He²,

Zhang³

et al. 2021

FEBS Open Bio

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Hypertrophic scaring (HS) is a dermal fibroproliferative disorder characterized by excessive deposition of collagen and other extracellular matrix (ECM) components. The aim of this study is to explore crucial lncRNAs and circRNAs associated with HS and provide a better understanding of the molecular mechanism of HS. To investigate the lncRNA, circRNA and mRNA expression profiles we performed RNA-sequencing of human HS and normal skin tissues. Following the identification of differentially expressed mRNAs (DEmRNAs), lncRNAs (DElncRNAs) and circRNAs (DEcircRNAs), we performed functional enrichment of DEmRNAs. Further on, we constructed DElncRNA/DEcircRNA-DEmRNA co-expression networks and ceRNA regulatory networks and performed functional analyses of the DEmRNAs in the constructed networks. In total, 487 DEmRNAs, 92 DElncRNAs and 17 DEcircRNAs were identified. DEmRNAs were significantly enriched in processes like collagen fibril organization, ECM-receptor interaction and PI3K-Akt signaling pathway. Additionally, we detected 580 DElncRNA-DEmRNA and 505 DEcircRNA-DEmRNA co-expression pairs The ceRNA network contained 18 circRNA-miRNA pairs, 18 lncRNA-miRNA pairs and 409 miRNA-mRNA pairs, including 10 circRNAs, 5 lncRNAs, 15 miRNAs, and 160 mRNAs. We concluded that MIR503HG/hsa-miR-204-3p/ACAN, MIR503HG/hsa-miR-431-5p/TNFRSF9, MEG3/hsa-miR-6884-5p/ADAMTS14, AC000035.1-ADAMTS14 and hsa_circ_0069865-COMP/ADAM12 interaction pairs may play a central role in HS.

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lncRNA MIR503HG functioned as a tumor suppressor and inhibited cell proliferation, metastasis and epithelial‐mesenchymal transition in bladder cancer

Cited by 32 publications

References 25 publications

<p>LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3</p>

<p>LncRNA miR503HG Regulates the Drug Resistance of Recurrent Cervical Squamous Cell Carcinoma Cells by Regulating miR-155/Caspase-3</p>

LncRNA MBNL1‐AS1 represses cell proliferation and enhances cell apoptosis via targeting miR‐135a‐5p/PHLPP2/FOXO1 axis in bladder cancer

Identification of crucial noncoding RNAs and mRNAs in hypertrophic scars via RNA sequencing

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