TCEA3 binds to TGF-beta receptor I and induces Smad-independent, JNK-dependent apoptosis in ovarian cancer cells

Cha, Young; Kim, Dae-Kwan; Hyun, Ja-Shil; Kim, Seong‐Jin; Park, Kyung-Soon

doi:10.1016/j.cellsig.2013.01.016

Cited by 28 publications

(27 citation statements)

References 23 publications

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“…Correspondingly, analysis through the SI module for splice junction arrays by AltAnalyze of RNA samples produced from primary neurons of mice with ablated (KO) FUS or HNRNPA1 [89] detected 147 exclusion events (Table S7B). The identified genes included IMPA2, which is associated with schizophrenia and bipolar disorder [90], the enolase NO1 which is differentially expressed under stress [91], Mclf2, a rho guanine nucleotide exchange factor that interacts with the mental retardation and autism related gene interleukin-1 accessory protein-like 1 (Il1RAPL1), TMPR555, a trans-membrane serine protease whose presynaptic distribution on motor neurons in the spinal cord suggests an important role in neural development [92] and the JNK signaling pathway activator TCEA3 [93]. Additionally, splicing alterations of HNRNPA1 were previously associated with selective loss of HNRNP A/B and with massive exon inclusions in AD entorhinal cortex, and lentiviral-mediated suppression of HNRNP A/B impaired electrocorticography in the mouse brain [79].…”

Section: Resultsmentioning

confidence: 99%

Long Non-Coding RNA and Alternative Splicing Modulations in Parkinson's Leukocytes Identified by RNA Sequencing

et al. 2014

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The continuously prolonged human lifespan is accompanied by increase in neurodegenerative diseases incidence, calling for the development of inexpensive blood-based diagnostics. Analyzing blood cell transcripts by RNA-Seq is a robust means to identify novel biomarkers that rapidly becomes a commonplace. However, there is lack of tools to discover novel exons, junctions and splicing events and to precisely and sensitively assess differential splicing through RNA-Seq data analysis and across RNA-Seq platforms. Here, we present a new and comprehensive computational workflow for whole-transcriptome RNA-Seq analysis, using an updated version of the software AltAnalyze, to identify both known and novel high-confidence alternative splicing events, and to integrate them with both protein-domains and microRNA binding annotations. We applied the novel workflow on RNA-Seq data from Parkinson's disease (PD) patients' leukocytes pre- and post- Deep Brain Stimulation (DBS) treatment and compared to healthy controls. Disease-mediated changes included decreased usage of alternative promoters and N-termini, 5′-end variations and mutually-exclusive exons. The PD regulated FUS and HNRNP A/B included prion-like domains regulated regions. We also present here a workflow to identify and analyze long non-coding RNAs (lncRNAs) via RNA-Seq data. We identified reduced lncRNA expression and selective PD-induced changes in 13 of over 6,000 detected leukocyte lncRNAs, four of which were inversely altered post-DBS. These included the U1 spliceosomal lncRNA and RP11-462G22.1, each entailing sequence complementarity to numerous microRNAs. Analysis of RNA-Seq from PD and unaffected controls brains revealed over 7,000 brain-expressed lncRNAs, of which 3,495 were co-expressed in the leukocytes including U1, which showed both leukocyte and brain increases. Furthermore, qRT-PCR validations confirmed these co-increases in PD leukocytes and two brain regions, the amygdala and substantia-nigra, compared to controls. This novel workflow allows deep multi-level inspection of RNA-Seq datasets and provides a comprehensive new resource for understanding disease transcriptome modifications in PD and other neurodegenerative diseases.

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Section: Resultsmentioning

confidence: 99%

Long Non-Coding RNA and Alternative Splicing Modulations in Parkinson's Leukocytes Identified by RNA Sequencing

et al. 2014

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“…The activation of drug resistance-associated signaling pathways was reported to be an important indicator of tumor drug resistance (13). In the present study, the phosphorylation levels of Sma and Madrelated protein (Smad)2, STAT3 and STAT5 in A549/DDP cells was determined following miR-10a silencing.…”

Section: Mir-10a Silencing Suppresses the Drug Efflux Of A549/ddp Cellsmentioning

confidence: 84%

MicroRNA-10a silencing reverses cisplatin resistance in the A549/cisplatin human lung cancer cell line via the transforming growth factor-β/Smad2/STAT3/STAT5 pathway

Sun

Chen

et al. 2015

Molecular Medicine Reports

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Abstract. Lung cancer is one of the primary causes of mortality worldwide and drug resistance is the key contributing factor which results in the failure of lung cancer chemotherapy. Previous studies have shown that microRNA (miR)-10a was involved in the reversal of cisplatin (DDP) resistance in numerous types of tumors; however, the underlying mechanism of action of this remains to be fully elucidated. In the present study, miR-10a silencing in human DDP-resistant lung cancer A549/DDP cells was demonstrated to improve DDP sensitivity, apoptosis, intracellular rhodamine-123 content as well as the expression and activity of caspase-3/8. In addition, miR-10a suppressed the cellular expression of P-glycoprotein, multi-drug resistance protein (MDR) 1, MDR-associated protein 1, RhoE, B cell lymphoma-2 and survivin in A549/DDP cells. Furthermore, miR-10a silencing inhibited the secretion of transforming growth factor (TGF)-β, phosphorylation of Sma-and Mad-related protein (Smad)2, signal transducer and activator of transcription (STAT)3 and STAT5, the transcriptional activity of hypoxia-inducible factor and eukaryotic translation initiation factor 4E in human lung cancer A549/DDP cell line. These results therefore indicated that miR-10a may be a potential target for improving the effectiveness of lung cancer chemotherapy via regulation of the TGF-β/Smad2/STAT3/STAT5 pathway.

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“…In addition, our integrated analysis showed that three mRNAs, i.e. metastasis suppressor 1 ( MTSS1 ), transcription elongation factor A (SII), 3 ( TCEA3 ) and MAP/microtubule affinity‐regulating kinase 1 ( MARK1 ), which have been reported to contribute to the tumour suppression, are targets of miR‐137. In HCC and glioblastoma, MTSS1 expression has been shown to inhibit cell migration, invasion and tumour metastasis .…”

Section: Discussionmentioning

confidence: 94%

“…In HCC and glioblastoma, MTSS1 expression has been shown to inhibit cell migration, invasion and tumour metastasis . TCEA3 was shown to induce apoptosis via activation of the JNK pathway in ovarian cancer cells; further, knock‐down of this gene expression was shown to enhance cell proliferation and colony formation ability of non‐cancerous ovarian epithelial cells . MARK1 is a component of Hippo signalling pathway and regulates this signalling cascade via LKB1‐MARK signalling axis .…”

Section: Discussionmentioning

confidence: 99%

Prognostic relevance of miR‐137 in patients with hepatocellular carcinoma

Sakabe

Azumi

Umekita

et al. 2016

Liver International

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TCEA3 binds to TGF-beta receptor I and induces Smad-independent, JNK-dependent apoptosis in ovarian cancer cells

Cited by 28 publications

References 23 publications

Long Non-Coding RNA and Alternative Splicing Modulations in Parkinson's Leukocytes Identified by RNA Sequencing

Long Non-Coding RNA and Alternative Splicing Modulations in Parkinson's Leukocytes Identified by RNA Sequencing

MicroRNA-10a silencing reverses cisplatin resistance in the A549/cisplatin human lung cancer cell line via the transforming growth factor-β/Smad2/STAT3/STAT5 pathway

Prognostic relevance of miR‐137 in patients with hepatocellular carcinoma

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