Modulator-Dependent RBPs Changes Alternative Splicing Outcomes in Kidney Cancer
In this study, we use a computational framework to investigate the roles of certain genes, termed modulators, on changing RBPs’ effect on splicing regulation. A total of 1,040,254 modulator-mediated RBP-splicing interactions were identified, including 137 RBPs, 4,309 splicing events and 2,905 modulator candidates from TCGA-KIRC RNA sequencing data. Modulators function categories were defined according to the correlation changes between RBPs expression and their targets splicing outcomes. QKI, as one of the RBPs influencing the most splicing events, attracted our attention in this study: 2,014 changing triplets were identified, including 1,101 modulators and 187 splicing events. Pathway enrichment analysis showed that QKI splicing targets were enriched in tight junction pathway, endocytosis and MAPK signaling pathways, all of which are highly associated with cancer development and progression. This is the first instance of a comprehensive study on how alternative splicing outcomes changes are associated with different expression level of certain proteins, even though they were regulated by the same RBP. Our work may provide a novel view on understanding alternative splicing mechanisms in kidney cancer.
Despite the emphasis on randomized data to guide evidence-based practice, there is a notable lack of clinical trials to inform comparative effectiveness in surgical disciplines. Although this is multifactorial in nature, this paucity ultimately reflects the difficulty associated with conducting surgical trials, particularly in settings where event rates are low (eg, lymph node metastasis in M0 renal cell carcinoma) or when long follow-up is required, as with early-stage disease (eg, low-risk prostate cancer).
Publication date: Available online 23 May 2020Source: European UrologyAuthor(s): David J. Pinato
Conclusion: By linking the NSKCR to several Swedish national databases, a unique database for RCC research has been created. PMID: 32436435 [PubMed - as supplied by publisher]
CONCLUSIONS: RP11-567G11.1 accelerates the proliferative and invasive abilities of RCC through activating the Notch pathway. Our findings suggest that it may be a new therapeutic target for RCC. PMID: 32432737 [PubMed - in process]
Conclusions: Taken together, we identified the key iron metabolism-related and methylated genes for ccRCC through a comprehensive bioinformatics analysis. This study provides a reliable and robust gene signature for the prognostic predictor of ccRCC patients and maybe provides a promising treatment strategy for this lethal disease.
British Journal of Cancer, Published online: 22 May 2020; doi:10.1038/s41416-020-0890-yIdentification of low-dose multidrug combinations for sunitinib-naive and pre-treated renal cell carcinoma
In conclusion, the inhibition of cysteine cathepsins by the peptides was beneficial in terms of cancer aggressiveness; however, they could affect the overall expression of these proteases.
Condition: Primary Disease: Unresectable or Metastatic Renal Cell Carcinoma Focus of the Study:PFS Assessed by IRC Per RECIST 1.1 Intervention: Combination Product: Biological : Toripalimab Drug: Axitinib sunitinib Sponsor: Shanghai Junshi Bioscience Co., Ltd. Not yet recruiting
This article is protected by copyright. All rights reserved