12/5/2023 0 Comments 3d scatter plot ggplot2 in r![]() ![]() However, the relationship between m 7G-related lncRNAs and ccRCC prognosis was unclear. Recently, lncRNAs were involved in the progression of malignancies according to other aticle, including kidney cancer 15, papillary thyroid tumors 16. Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts longer than 200 nucleotides 14. Modification of m 7G and atypical expression of lncRNAs may result in different diseases, including many types of cancer. m 7G modification exerts important effects on liver cancer 12, cardiovascular disease 13, clear cell kidney cancer 9, growth, invasion, and metastasis. Most tRNAs are modified at nucleotide 46 11 in the variable loop to improve stability. Interestingly, m 7G tRNA modification enhances the mRNA translation of oncogenes 8 and is strongly associated with the development of ccRCC 9 and multiple tumors.ħ-methylguanosine (m 7G) is a type of RNA methylation and is generated by the methylation of a guanosine base at the N-7 position 10. ![]() To better understand the molecular mechanisms of ccRCC and improve early diagnosis and treatment, it remains imperative to identify new diagnostic, therapeutic, and prognostic markers. Moreover, ccRCC is resistant to existing therapies such as chemotherapy, interferon immunotherapy (IFN-α), tyrosine kinase inhibitor targeted therapy, and mammalian targets of the rapamycin pathway 5, 6, 7. However, 30% of patients experience recurrence or metastasis after surgery 4. ![]() Radiogenomics 2 and the combination of Radiomics and artificial intelligence (AI) 3 of ccRCC have contributed in trying to improve diagnosis and treatment. Current treatments for ccRCC include partial nephrectomy, radical nephrectomy, targeted drug therapy and immunotherapy. Kidney cancer is among the most aggressive type of the urinary system worldwide 1, ccRCC subtype is the most common pathological classification of renal tumors. This risk model may be promising for the clinical prediction of prognosis and immunotherapeutic responses in patients with ccRCC. Quantitative real-time polymerase chain reaction (qRT-PCR) exhibited that the expression levels of LINC01507, AC093278.2 were very high in all five ccRCC cell lines, AC084876.1 was upregulated in all ccRCC cell lines except 786-O, and the levels of AL118508.1 and DUXAP8 were upregulated in the Caki-1 cell line. Moreover, a lower tumor mutation burden combined with low-risk scores was associated with a better prognosis of ccRCC. High-risk group of patients was more susceptible to A.443654, A.770041, ABT.888, AMG.706, and AZ628. The IC 50 value for drug sensitivity divided patients into two risk groups. Principal component analysis (PCA) indicated that the risk model precisely separated the patients into different groups. In all, a model based on five lncRNAs was developed. Furthermore, we performed Kaplan–Meier analysis and area under the curve (AUC) analysis for diagnosis. A prognostic multi-lncRNA signature was created using LASSO regression to examine the differential expression of m7G-related lncRNAs in ccRCC. However, knowledge of N 7-methylguanosine (m 7G)-related lncRNAs that predict ccRCC prognosis remains insufficient. Clear cell renal cell carcinoma (ccRCC) is regulated by methylation modifications and long noncoding RNAs (lncRNAs).
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