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ELOVL5 promotes cell proliferation and invasion in renal cell carcinoma

ABSTRACT: ELOVL5 promotes cell proliferation and invasion in renal cell carcinoma

PROVIDER: PRJNA791351 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17297700_1.fastq.gz	Fastqsanger.gz
	SRR17297700_2.fastq.gz	Fastqsanger.gz
	SRR17297701_1.fastq.gz	Fastqsanger.gz
	SRR17297701_2.fastq.gz	Fastqsanger.gz
	SRR17297702_1.fastq.gz	Fastqsanger.gz

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ELOVL5 promotes cell proliferation and invasion in renal cell carcinoma

Project description:Fatty acid is a main component of lipid. The differences of chain-length and pattern of saturation / desaturation in fatty acid are essential for diversity of biological lipid functions. Elongation of very-long-chain fatty acids (ELOVL) plays a critical role in regulating the elongation of fatty acid and ELOVL 1 to 7 are reported in the present. In several cancers but renal cell carcinoma (RCC), the relationship between ELOVLs and cancer progression has been reported. In TCGA cohort, ELOVL5 expression is associated with advanced TNM stage and poor prognosis. We performed CRISPR-Cas9 targeted knockout of ELOVL5 in 2 different RCC cell lines, ACHN and 786-O, respectively. ELOVL5 knockout significantly suppressed cellular invasion, migration and proliferation in vitro and in vivo. In ingenuity Pathway Analysis, Akt signaling activation was decreased in ELOVL5-KO cells. In western blotting analysis, the phosphorylation level of Akt was inhibited in ELOVL5-KO cells. Resultantly, it was suggested that ELOVL5 is involved in the phosphorylation level of Akt and affects cancer progression in RCC.

2022-08-17 | GSE192403 | GEO

NUF2-HMGA2 axis drives cell proliferation, migration, and invasion in clear cell renal cell carcinoma

Project description:NUF2-HMGA2 axis drives cell proliferation, migration, and invasion in clear cell renal cell carcinoma

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NUF2-HMGA2 axis drives cell proliferation, migration, and invasion in clear cell renal cell carcinoma

Project description:The relatively poor sensitivity of clear cell renal cell carcinoma (ccRCC) to conventional chemotherapy and radiotherapy makes its treatment challenging. The Ndc80 kinetochore complex component (NUF2) is involved in the development and progression of several cancers. However, its role in ccRCC remains unclear. In an effort to identify novel treatment targets and prognostic markers for ccRCC, we investigated the role of NUF2 in ccRCC progression. We found that the expression of NUF2 was increased in ccRCC tissues and cells, and the elevated NUF2 levels were significantly associated with worse clinicopathological parameters and shorter survival. In addition, NUF2 was an independent prognostic biomarker for ccRCC. Knocking down NUF2 expression affected the proliferation, migration, and invasion of ccRCC cells and the expression of epithelial–mesenchymal transition (EMT)-related markers. Moreover, RNA sequencing and in vitro experiments identified the oncogene high-mobility group AT-hook 2 (HMGA2) as the target factor regulated by NUF2 in ccRCC. Restoring HMGA2 levels ameliorated the inhibitory effects of NUF2 depletion on cell proliferative, migratory, and invasive capacities and recovered the expression of EMT-related markers to basal levels.These results suggest that NUF2 promotes proliferation, migration, and invasion of ccRCC cells, at least partly by regulating HMGA2, and that the NUF2-HMGA2 axis could be an ideal therapeutic target and a promising prognostic indicator for ccRCC.

2022-06-30 | GSE192754 | GEO

KIAA1429 promotes cell proliferation by regulating MYC messenger RNA in clear cell renal cell carcinoma

Project description:KIAA1429 is an integral component of the m6A methyltransferase complex, essential for facilitating the interaction between the catalytic core components METTL3 and METTL14. However, the mechanisms by which KIAA1429 influences clear cell Renal cell carcinoma (ccRCC) remain incompletely elucidated. Analysis of the TCGA and GEO database confirmed that KIAA1429 was significantly upregulated in ccRCC samples, which correlated with poor survival. Additionally, qRT-PCR, Western Blot and IHC detection revealed significantly upregulated levels of KIAA1429 in ccRCC tissues. Moreover, multivariable Cox regression analysis showed that patients with ccRCC with high KIAA1429 expression had a poor clinical prognosis. Notably, silencing KIAA1429 significantly inhibited the proliferation, migration and invasion of ccRCC cells. Similarly, KIAA1429 knockdown also significantly inhibited the growth of ccRCC cells in nude mice. Mechanistically, KIAA1429 silencing significantly reduced the overall level of m6A in, the stability of MYC mRNA and the mRNA and protein expressions of MYC in ccRCC cells. Furthermore, RIP-qRT-PCR experiments showed that KIAA1429 could directly bind to MYC mRNA. MeRIP assay revealed that KIAA1429 knockdown resulted in a significant decrease in the m6A level of MYC mRNA in ccRCC cells. In conclusion, KIAA1429 regulates the proliferation, migration and invasion of ccRCC cells by stabilizing MYC mRNA in an m6A-dependent manner. Therefore, targeting the KIAA1429-MYC signalling pathway emerges as a potential strategy for the treatment of renal cell carcinoma.

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Project description:<h4><strong>BACKGROUND:</strong> Elevated choline kinase alpha (ChoK) is observed in most solid tumours including glioblastomas (GBM), yet until recently, inhibitors of ChoK have demonstrated limited efficacy in GBM models. Given that hypoxia is associated with GBM therapy resistance, we hypothesised that tumour hypoxia could be responsible for such limitations. We therefore evaluated in GBM cells, the effect of hypoxia on the function of JAS239, a potent ChoK inhibitor.</h4><h4><strong>METHODS:</strong> Rodent (F98 and 9L) and human (U-87 MG and U-251 MG) GBM cell lines were subjected to 72 hours of hypoxia conditioning and treated with JAS239 for 24 hours. NMR metabolomic measurements and analyses were performed to evaluate the signalling pathways involved. In addition, cell proliferation, cell cycle progression and cell invasion were measured in cell monolayers and 3D spheroids, with or without JAS239 treatment in normoxic or hypoxic cells to assess how hypoxia affects JAS239 function.</h4><h4><strong>RESULTS:</strong> Hypoxia and JAS239 treatment led to significant changes in the cellular metabolic pathways, specifically the phospholipid and glycolytic pathways associated with a reduction in cell proliferation via induced cell cycle arrest. Interestingly, JAS239 also impaired GBM invasion. However, JAS239 effects were variable depending on the cell line, reflecting the inherent heterogeneity observed in GBMs.</h4><h4><strong>CONCLUSION:</strong> Our findings indicate that JAS239 and hypoxia can deregulate cellular metabolism, inhibit proliferation and alter cell invasion. These results may be useful for the design of new therapeutic strategies based on ChoK inhibition that can act on multiple pro-tumorigenic features.</h4>

2024-06-18 | MTBLS6212 | MetaboLights

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