Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells

Hu, Zhiyan; Wang, Xiaoyan; Guo, Wenbin; Xie, Linying; Huang, Yuqi; Liu, Yan-Ping; Xiao, Liwei; Li, Shengnan; Zhu, Hui; Li, Zuguo; Kan, Heping

doi:10.18632/oncotarget.7367

Cited by 58 publications

(48 citation statements)

References 26 publications

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“…The MALAT1 gene is highly conserved across mammals, suggesting that it may have important biological implications [9]. Evidence suggests that MALAT1 may act like an oncogene in several malignancies, including lung cancer [17, 24], pancreatic cancer [19], liver cancer [20], bladder cancer [25], prostate cancer[26], colon cancer [27, 28], renal cell carcinoma [18], and oral squamous cell carcinomas [29, 30]. Lowering MALAT1 expression in hepatocellular carcinoma cells resulted in reduced cell proliferation and colony formation [20].…”

Section: Discussionmentioning

confidence: 99%

“…Lowering MALAT1 expression in hepatocellular carcinoma cells resulted in reduced cell proliferation and colony formation [20]. MALAT1 was also found to promote colon cancer cell proliferation, invasion and metastasis in vitro and in vivo by increasing AKAP-9 expression [28]. For breast cancer, suppressing MALAT1 expression led to increased differentiation of primary tumor cells and reduced metastasis [31].…”

Section: Discussionmentioning

confidence: 99%

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High expression of long non-coding RNA MALAT1 in breast cancer is associated with poor relapse-free survival

Wang

Katsaros²,

Biglia³

et al. 2018

Breast Cancer Res Treat

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

High expression of long non-coding RNA MALAT1 in breast cancer is associated with poor relapse-free survival

Wang

Katsaros²,

Biglia³

et al. 2018

Breast Cancer Res Treat

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“…Derived from normal colon epithelial cells, colorectal cancer (CRC) has been regarded as a malignant cancer, which causes massive morbidity and mortality all over the world (Chubb et al, ; Hu et al, ). Millions of people suffer from the threat of CRC (Wang, Nie, Wu, Liu, & Guo, ; J. Zhang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Ren

Zheng-jun

et al. 2019

Journal Cellular Physiology

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Colorectal cancer (CRC), is mostly derived from normal colon epithelial cells, and has been reported to be one of most common gastrointestinal malignancies globally. An increasing number of researchers have claimed that long noncoding RNAs (lncRNAs) exert significant functions in tumor progression. Nevertheless, the function of MAGI2-AS3 remains uncertain in CRC. The expression of MAGI2-AS3, miR-3163, and transmembrane protein 106B (TMEM106B) messenger RNA was examined by quantitative real-time polymerase chain reaction. Cell apoptosis was measured by caspase-3 activity test. Cell proliferation was tested by cell-counting kit 8 and 5-ethynyl-2′-deoxyuridine assays. Cell migration was detected by transwell assay. Western blot analysis examined the protein expression of TMEM106B. The expression of Ki-67 was evaluated by immunohistochemistry assay. The binding capacity between miR-3163 and MAGI2-AS3 (or TMEM106B) was studied by radioimmunoprecipitation and luciferase reporter assays. The expression of MAGI2-AS3 and TMEM106B was conspicuously upregulated whereas miR-3163 presented lower expression in CRC cells. MAGI2-AS3 deficiency facilitated cell apoptosis but hampered cell proliferation and migration. MAGI2-AS3 combined with miR-3163 and negatively regulated miR-3163 expression. In addition, the administration of sh-MAGI2-AS3 or miR-3163 mimics suppressed CRC cell growth in vivo. Subsequently, miR-3163 targeted TMEM106B and the transfection of sh-MAGI2-AS3 or miR-3163 mimics downregulated TMEM106B expression. Rescue assays verified that TMEM106B overexpression recovered the effects of MAGI2-AS3 inhibition on cell apoptosis, proliferation, and migration in CRC. MAGI2-AS3 drives CRC progression through regulating miR-3163/TMEM106B axis. This supplies innovative insights on the investigation of molecular mechanism in CRC progression. K E Y W O R D S CRC, MAGI2-AS3, miR-3163, TMEM106B

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“…Such as, previous studies suggested that long non-coding RNA MALAT1 promoted tumor growth and metastasis by inducing epithelial-mesenchymal transition in oral squamous cell carcinoma [10]. MALAT1 increased AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells [11]. Wang et al reported that MALAT1 promoted malignant development of esophageal squamous cell carcinoma by targeting β-catenin via Ezh2 [12].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MALAT1 drives gastric cancer progression by regulating HMGB2 modulating the miR-1297

Gao

Tian

et al. 2017

Cancer Cell Int

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BackgroundEmerging evidences have verified that long non-coding RNAs (lncRNAs) play important regulatory roles in the pathogenesis and progression of cancers. lncRNAs metastasis associated lung adenocarcinoma transcript 1 (MALAT1) have been found to be up-regulated in some human cancers. The main objective of this study was to investigate the expression level and biological function of MALAT1 in gastric cancer (GC).MethodsQuantificational real-time polymerase chain reaction (qRT-PCR) was performed to detect the mRNA levels of MALAT1 in 78 paired gastric carcinoma tissues and adjacent normal tissues, and the associations of MALAT1 expression with the clinicopathological features were analyzed, and the prognosis of gastric carcinoma patients was evaluated. The HMGB2 mRNA and protein expressions were detected by qRT-PCR and western-blot analysis. Luciferase reporter assay was used to determine miR-1297 was a target of MALAT1.ResultsIn this study, we demonstrated MALAT1 was up-regulation in GC tissues compared with adjacent normal tissues and higher MALAT1 expression was correlated with local invasion, lymph node metastasis and TNM stage. Patients with higher MALAT1 expression predicted a shorter survival and poor prognosis. Functionally, we revealed that MALAT1 promoted cells proliferation and invasion in GC. Mechanistically, our results demonstrated that MALAT1 was negatively correlation with miR-1297 and functioned as a molecular sponging miR-1297, antagonizing its ability to suppress HMGB2 expression.ConclusionsTaken together, these results demonstrated that MALAT1/miR-1297/HMGB2 axis acted as critical regulator pathway in GC tumorigenesis and progression, which provided a novel therapeutic target for gastric cancer.

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Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells

Cited by 58 publications

References 26 publications

High expression of long non-coding RNA MALAT1 in breast cancer is associated with poor relapse-free survival

High expression of long non-coding RNA MALAT1 in breast cancer is associated with poor relapse-free survival

Long noncoding MAGI2‐AS3 promotes colorectal cancer progression through regulating miR‐3163/TMEM106B axis

Long non-coding RNA MALAT1 drives gastric cancer progression by regulating HMGB2 modulating the miR-1297

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