LncRNA and mRNA expression of cisplatin-resistant versus parental SCC9 cells
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PROVIDER: PRJNA437468 | ENA |
REPOSITORIES: ENA
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Project description:Increasing evidence has shown that chemoresistance is related to the process of epithelial-mesenchymal transition (EMT) and increased invasiveness by tongue squamous cell carcinoma (TSCC) cells. Long noncoding RNAs (lncRNAs) play pivotal roles in tumour metastasis and progression. However, the roles and mechanisms of lncRNAs in cisplatin resistance induced EMT and metastasis are not well understood. In this study, a Chemotherapy Induced Long non-coding RNA 1 (CILA1) was discovered by using microarrays and was functionally identified as a regulator of chemo-sensitivity in TSCC cells.Upregulation of CILA1 promotes EMT, invasiveness and chemoresistance in TSCC cells, whereas the inhibition of CILA1 expression induces MET and chemosensitivity and inhibis the invasiveness of cisplatin-resistant cells both in vitro and in vivo. We also found that CILA1 exerts its functions via the activation of the Wnt/ β-catenin signalling pathway.High CILA1 expression levels and low levesl of phosphorylated β-catenin were closely associated with cisplatin-resistance and advanced disease stage, and were predictors of poor prognosis in TSCC patients. These findings provided a new biomarker for Increasing evidence has shown that chemoresistance is related to the process of epithelial-mesenchymal transition (EMT) and increased invasiveness by tongue squamous cell carcinoma (TSCC) cells. Long noncoding RNAs (lncRNAs) play pivotal roles in tumour metastasis and progression. However, the roles and mechanisms of lncRNAs in cisplatin resistance induced EMT and metastasis are not well understood. In this study, a Chemotherapy Induced Long non-coding RNA 1 (CILA1) was discovered by using microarrays and was functionally identified as a regulator of chemo-sensitivity in TSCC cells.Upregulation of CILA1 promotes EMT, invasiveness and chemoresistance in TSCC cells, whereas the inhibition of CILA1 expression induces MET and chemosensitivity and inhibis the invasiveness of cisplatin-resistant cells both in vitro and in vivo. We also found that CILA1 exerts its functions via the activation of the Wnt/ β-catenin signalling pathway.High CILA1 expression levels and low levesl of phosphorylated β-catenin were closely associated with cisplatin-resistance and advanced disease stage, and were predictors of poor prognosis in TSCC patients. These findings provided a new biomarker for the chemosensitivity of TSCC tumours and a therapeutic target for TSCC treatment.
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Project description:Chemoresistance frequently leads to therapeutic failure in tongue squamous cell carcinoma (TSCC). Increasing evidence has shown that Long noncoding RNAs (lncRNAs) play pivotal roles in biological properties of cancer. However, the roles and mechanisms of lncRNAs in cisplatin resistance are not well understood. In this study, to identify the lncRNAs induced by chemotherapy, we profile the expression of lncRNAs in cisplatin-resistant TSCC cells using LncRNA microarrays.
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Project description:Chemoresistance frequently leads to therapeutic failure in oral squamous cell carcinoma (OSCC). While miRNA have been widely reported having global regulatory roles in cancer biological properties, yet their localiztion alteration under cisplatin treatment has not been clarified. In this study, to identify the sublocalization characteristics of miRNAs induced by chemotherapy, especially the specific mitochondrial localization of miRNA, we profile the expression of miRNAs in cisplatin-resistant and parental TSCC cells using miRNA microarrays.
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Project description:The development of chemo-resistance has dramatically limited the clinical efficiency of platinum-based therapy. Although many resistant mechanisms have been demonstrated, genetic/molecular alterations responsible for drug resistance in the majority of clinical cases has not been identified. We analyzed three pairs of testicular germ cell tumor (TGCT) cell lines using Affymetrix expression microarrays to identify differential expressed genes. Then the expression of CCND1/CyclinD1, selected from the microarray analysis, was determined in cisplatin sensitive and resistance cancer samples including TGCTs, ovarian and prostate cancers by quantitative reverse transcription PCR analysis (qRT-PCR). Finally, we determined the gene knocked-down effect of CyclinD1. Expression microarray study revealed a limited number of differentially expressed genes across all three cell lines when comparing the parental and resistant cells. Among them, CyclinD1 was the most significantly differentially expressed gene. Importantly, we found that, in clinical TGCT samples, the overall expression level of cyclinD1 is higher in resistant cases compared to those sensitive samples (9/12 in the resistant group and only 3/8 in the sensitive group). We also found that cyclinD1 expressed dozens of fold higher in the resistant than in the sensitive ovarian cancer cell lines and dramatically overexpressed in prostate cancer. We re-sensitized the resistant cells by knocking-down cyclinD1. We demonstrated that deregulation of cyclinD1 is the major cause of TGCT cisplatin resistance and it may also be commonly involved in other human cancers. Combined cyclinD1 inhibition and cisplatin chemotherapy may be used clinically to treat the large number of cyclinD1 deregulated resistant tumors. RNA from three paired parental and cisplatin-resistant TGCT cell lines was extracted and analysed by Affymetrix gene expression microarray profiling (Human Genome U133 plus 2.0 arrays). Expression changes associated with the resistant phenotype were identified by comparing the three cisplatin-resistant derivatives to their parental counterparts.
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