Preliminary study on the role of the C5orf46 gene in renal cancer.
Biomarker
C5orf46
Immune cells
Prognostic
Renal cancer
Journal
Translational oncology
ISSN: 1936-5233
Titre abrégé: Transl Oncol
Pays: United States
ID NLM: 101472619
Informations de publication
Date de publication:
Jul 2022
Jul 2022
Historique:
received:
04
03
2022
revised:
15
04
2022
accepted:
24
04
2022
pubmed:
4
5
2022
medline:
4
5
2022
entrez:
3
5
2022
Statut:
ppublish
Résumé
C5orf46 has been found to have antibacterial and anti-inflammatory effects via sequencing and microarray technologies, but its effects on cancer are unclear. C5orf46 expression in renal cancer patients and cell lines was measured by quantitative polymerase chain reaction (qPCR). RNA sequencing data and clinicopathological information from renal cancer patients extracted from The Tumor Genome Atlas (TCGA) were analyzed to evaluate the prognostic value of C5orf46. The role of C5orf46 in vitro was verified by migration, proliferation and apoptosis experiments in renal cancer cell lines. Furthermore, the transcriptome of renal cancer cell lines with C5orf46 knocked down was sequenced to analyze potential signaling network pathways. Finally, the possible mechanisms of C5orf46 involvement in renal cancer development were analyzed by evaluating the immune microenvironment, mutation status and methylation levels. C5orf46 was highly expressed in renal cancer and was an independent prognostic factor. In vitro cell experiments showed that inhibition of C5orf46 expression could reduce renal cancer cell proliferation and migration and increase apoptosis. Transcriptomic sequencing after knockdown of C5orf46 in renal cancer cells revealed that it is involved in the malignant phenotype and immune microenvironment regulation of renal cancer. Finally, public databases suggest that C5orf46-related immune cell infiltration, mutational potential, and low methylation levels may contribute to poor prognosis in renal cancer. These findings suggest that C5orf46 is associated with renal cancer progression and could be a potential target for improving renal cancer prognosis.
Sections du résumé
BACKGROUND
BACKGROUND
C5orf46 has been found to have antibacterial and anti-inflammatory effects via sequencing and microarray technologies, but its effects on cancer are unclear.
METHODS
METHODS
C5orf46 expression in renal cancer patients and cell lines was measured by quantitative polymerase chain reaction (qPCR). RNA sequencing data and clinicopathological information from renal cancer patients extracted from The Tumor Genome Atlas (TCGA) were analyzed to evaluate the prognostic value of C5orf46. The role of C5orf46 in vitro was verified by migration, proliferation and apoptosis experiments in renal cancer cell lines. Furthermore, the transcriptome of renal cancer cell lines with C5orf46 knocked down was sequenced to analyze potential signaling network pathways. Finally, the possible mechanisms of C5orf46 involvement in renal cancer development were analyzed by evaluating the immune microenvironment, mutation status and methylation levels.
RESULTS
RESULTS
C5orf46 was highly expressed in renal cancer and was an independent prognostic factor. In vitro cell experiments showed that inhibition of C5orf46 expression could reduce renal cancer cell proliferation and migration and increase apoptosis. Transcriptomic sequencing after knockdown of C5orf46 in renal cancer cells revealed that it is involved in the malignant phenotype and immune microenvironment regulation of renal cancer. Finally, public databases suggest that C5orf46-related immune cell infiltration, mutational potential, and low methylation levels may contribute to poor prognosis in renal cancer.
CONCLUSION
CONCLUSIONS
These findings suggest that C5orf46 is associated with renal cancer progression and could be a potential target for improving renal cancer prognosis.
Identifiants
pubmed: 35504177
pii: S1936-5233(22)00101-2
doi: 10.1016/j.tranon.2022.101442
pmc: PMC9079122
pii:
doi:
Types de publication
Journal Article
Langues
eng
Pagination
101442Informations de copyright
Copyright © 2022. Published by Elsevier Inc.
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