lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

Xu, Jiheng; Yang, Rui; Hua, Xiaohui; Huang, Maowen; Tian, Zhongxian; Li, Jingxia; Lam, H.; Jiang, Guosong; Cohen, Mitchell D.; Huang, Chuanshu

doi:10.1016/j.omtn.2020.06.010

Cited by 27 publications

(19 citation statements)

References 71 publications

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“…34 This phenomenon could be activated or restrained by various types of modifications, such as phosphorylation or glycosylation. 35,36 Xu et al 37 TGF-β1 at the transcriptional level. 28 This phenomenon indicated that SNHG17-recruited c-Jun triggers TGF-β1-induced SNHG17.…”

Section: Discussionmentioning

confidence: 99%

SNHG17, as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma

Shen

Liang

et al. 2021

Cancer Science

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Esophageal cancer is one of the most common gastrointestinal tumors worldwide, ranking seventh in incidence and sixth in cancer-related mortality in 2018. 1 The main types of esophageal cancers are ESCC and esophageal adenocarcinoma (EAC). 2 ESCC is the predominant histological type of esophageal cancer in China. 3 The geographical variation in the incidence is striking, exhibiting a high prevalence in the Taihang mountain region in north-central China, such as Cixian in Hebei, Henan, and Shanxi provinces. 4 Although there have been great advances in the treatment of esophageal cancer, patients with ESCC experience malignant proliferation and invasion, leading to poor survival (5-y survival rate <30%). 5,6 Therefore, understanding the ESCC progression mechanism to improve the clinical outcome of patients with ESCC is essential.

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Section: Discussionmentioning

confidence: 99%

SNHG17, as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma

Shen

Liang

et al. 2021

Cancer Science

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“…Mechanistically, SOX2OT upregulates SOX2 expression by sponging miR-200c 10 . In addition, many lncRNAs such as CASC9 42 , SNHG1 43 , TUG1 44 , and NBAT1 45 are associated with the occurrence and development of bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis

et al. 2020

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Apart from being potential prognostic biomarkers and therapeutic targets, long non-coding RNAs (lncRNAs) modulate the development and progression of multiple cancers. PlncRNA-1 is a newly discovered lncRNA that exhibits the above properties through multiple regulatory pathways. However, the clinical significance and molecular mechanisms of PlncRNA-1 in bladder cancer have not been established. PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues. Moreover, the expression level correlated with tumor invasion, T stage, age, and number of tumors, but not with gender, recurrent status, preoperative treatment, pathological grade, and tumor size. The expression level of PlncRNA-1 can, to a certain extent, be used as a predictor of the degree of tumor invasion and T stage among BC patients. Inhibiting PlncRNA-1 expression impaired the proliferation, migration, and invasion of T24 and 5637 bladder cancer cells in vitro and in vivo. Specifically, PlncRNA-1 promoter in BC tissues was found to be hypomethylated at position 131 (36157603 on chromosome 21). PlncRNA-1 promoter hypomethylation induces the overexpression of PlncRNA-1. In addition, PlncRNA-1 modulated the expression of smad3 and has-miR-136-5p (miR-136). Conversely, miR-136 regulated the expression of PlncRNA-1 and smad3. PlncRNA-1 mimics competitive endogenous RNA (ceRNA) in its regulation of smad3 expression by binding miR-136. Rescue analysis further revealed that modulation of miR-136 could reverse the expression of smad3 and epithelial–mesenchymal transition (EMT) marker proteins impaired by PlncRNA-1. In summary, PlncRNA-1 has important clinical predictive values and is involved in the post-transcriptional regulation of smad3. The PlncRNA-1/miR-136/smad3 axis provides insights into the regulatory mechanism of BC, thus may serve as a potential therapeutic target and prognostic biomarker for cancer.

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“…Of note, a large number of lncRNAs have been found to play an important role in invasion, metastasis and drug resistance in BC [8][9][10]. For instance, lncRNA-SNHG1 promotes basal MIBC cell invasion by interacting with the PP2A catalytic subunit and inducing autophagy [11]. LncRNA-SLC16A1-AS1 induces metabolic reprogramming as a target and coactivator of E2F1 in BC progression [12].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis

Xiao

Zuo

et al. 2022

Preprint

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BackgroundBladder cancer (BC) is the most common genitourinary malignancy worldwide, and its aetiology and pathogenesis remain unclear. Long noncoding RNAs can play vital roles in gene expression and diverse biological processes, especially in cancers. Accumulating evidence has shown that HAGLROS, a novel lncRNA, is closely related to the occurrence and progression of various cancers. However, the biological functions and underlying mechanisms of HAGLROS in BC remain unknown.MethodsThe relative expression of HAGLROS in BC was determined by bioinformatics analysis, transcriptome sequencing analysis and qRT–PCR. Gain- or loss-of-function assays were performed to study the biological roles of HAGLROS in BC. A CCK-8 assay was used to detect BC cell proliferation. BC cell invasion and migration were investigated by wound healing and Transwell assays. The cell cycle was analysed by flow cytometry assay. Western blot analysis and immunohistochemistry were performed to evaluate SPRR1B expression. The differential expression of candidate genes and their relationships were evaluated in data retrieved from the starBase database, the GEIPIA database, the Lnc2Cancer database and the LncBase database. FISH assays, subcellular fractionation assays and luciferase reporter assays were performed to explore the underlying molecular mechanisms of HAGLROS.ResultsHAGLROS expression is significantly upregulated in BC tissues and cells, and increasing HAGLROS expression was related to high pathologic grade. HAGLROS enhances the proliferation, migration and invasion of BC. Furthermore, SPRR1B is obviously upregulated and miR-330-5p is significantly downregulated in BC. Mechanistically, we found that HAGLROS is mainly located in the cytoplasm and positively regulates SPRR1B expression by sponging miR-330-5p, playing an oncogenic role in BC pathogenesis.ConclusionsThe present study demonstrates that HAGLROS is significantly overexpressed and plays an oncogenic role by regulating the miR-330-5p/SPRR1B axis in BC. HAGLROS may serve as a potential biomarker for the diagnosis and treatment of BC.

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lncRNA SNHG1 Promotes Basal Bladder Cancer Invasion via Interaction with PP2A Catalytic Subunit and Induction of Autophagy

Cited by 27 publications

References 71 publications

SNHG17, as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma

SNHG17, as an EMT‐related lncRNA, promotes the expression of c‐Myc by binding to c‐Jun in esophageal squamous cell carcinoma

Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis

Long Non-Coding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis

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