Molecular mechanism of SNHG11 in human osteosarcoma cells
Data files
Nov 20, 2024 version files 65.40 GB
-
1_human-NC_2-mRNA.fq.gz
2.61 GB
-
2_human-NC_2-mRNA.fq.gz
2.58 GB
-
README.md
963 B
-
SNHG11_Input1-1_R1_001.fastq.gz
2.10 GB
-
SNHG11_Input1-1_R2_001.fastq.gz
2.17 GB
-
SNHG11_Input1-2_R1_001_all.fastq.gz
1.66 GB
-
SNHG11_Input1-2_R2_001_all.fastq.gz
1.74 GB
-
SNHG11_Input2-1_R1_001.fastq.gz
2.22 GB
-
SNHG11_Input2-1_R2_001.fastq.gz
2.29 GB
-
SNHG11_Input2-2_R1_001_all.fastq.gz
1.47 GB
-
SNHG11_Input2-2_R2_001_all.fastq.gz
1.53 GB
-
SNHG11_pulldown1-1_R1_001.fastq.gz
2.55 GB
-
SNHG11_pulldown1-1_R2_001.fastq.gz
2.93 GB
-
SNHG11_pulldown1-2_R1_001.fastq.gz
1.30 GB
-
SNHG11_pulldown1-2_R2_001.fastq.gz
1.37 GB
-
SNHG11_pulldown2-1_R1_001.fastq.gz
2.02 GB
-
SNHG11_pulldown2-1_R2_001.fastq.gz
2.36 GB
-
SNHG11_pulldown2-2_R1_001.fastq.gz
1.52 GB
-
SNHG11_pulldown2-2_R2_001.fastq.gz
1.60 GB
-
U2OSOE-NC-1_R1_001.fastq.gz
2.79 GB
-
U2OSOE-NC-1_R2_001.fastq.gz
2.79 GB
-
U2OSOE-NC-3_R1_001.fastq.gz
2.86 GB
-
U2OSOE-NC-3_R2_001.fastq.gz
2.86 GB
-
U2OSOE-SNHG11-1_R1_001.fastq.gz
3.39 GB
-
U2OSOE-SNHG11-1_R2_001.fastq.gz
3.39 GB
-
U2OSOE-SNHG11-2_R1_001.fastq.gz
2.59 GB
-
U2OSOE-SNHG11-2_R2_001.fastq.gz
2.60 GB
-
U2OSOE-SNHG11-3_R1_001.fastq.gz
3.07 GB
-
U2OSOE-SNHG11-3_R2_001.fastq.gz
3.06 GB
Abstract
Osteosarcoma ( OS ) is a malignant bone tumor of mesenchymal origin, which is common in children and adolescents. LncRNA SNHG11 plays an important regulatory role in a variety of cancers and plays a key role in the migration, invasion, proliferation of a variety of cancer cells. At present, there is no report on the function and regulatory mechanism of lncRNA SNHG11 in osteosarcoma.We found Overexpression of SNHG11 inhibited the proliferation of in human osteosarcoma U2OS cells and promoted apoptosis.Overexpression of SNHG11 in U2OS cells resulted in significant differential expression of 344 genes, including 82 up-regulated genes and 262 down regulated genes.The upregulated differentially expressed genes were not enriched in relevant biological processes on GO-P, among which HMGCS2 and IL24 deserve attention.Downregulated genes are enriched in GO-P for cell adhesion and migration, among which KRT17, CXCL14, TRIB2, COL5A1, CCL24, SOX2, and COL6A3 are worth paying attention to. SNHG11 may interact with KRT6 B, SERPINB12 and DCD proteins to regulate downstream targets. ChIRP-seq ( RNA ) sequencing revealed that SNHG11 specifically binds to EEF2, RPS4X, and ACTG1. ChIRP-seq ( DNA ) sequencing showed that SNHG11 gene was mainly enriched in biological processes such as negative regulation of apoptosis process in GO-P. Integrated analysis of ChIRP-seq ( RNA ) revealed 32 overlapping genes, and SNHG11 may participate in the progression of osteosarcoma by binding to DCD and regulating these 32 target genes. Integrated analysis of ChIRP-seq ( DNA ) revealed 16 overlapping genes. Combined with the results of protein profiling, it is speculated that SNHG11 may be involved in the progression of osteosarcoma by binding SERPINB12 and regulating the transcription.LncRNA SNHG11 plays a key role in the development of osteosarcoma by affecting cell information carrier molecules at three levels of DNA, RNA and protein.
https://doi.org/10.5061/dryad.zgmsbccnm
Description of the data and file structure
This project aims to detect the effect of overexpression of lncRNA SNHG11 on the proliferation and apoptosis of U2OS cells in human osteosarcoma cells. And high-throughput transcriptome sequencing was used to obtain RNA seq and ChIRP seq data affected by SNHG11. Combined with bioinformatics analysis methods, the interacting proteins, RNA, and DNA targets of SNHG11 in U2OS cells were analyzed.
Code/software
Due to the possibility of errors during data transmission, in order to ensure that the data you downloaded is intact and undamaged, it is necessary to use md5 software to verify whether the md5 value of the file you received is consistent with the md5sum.exe we sent. Inconsistencies indicate errors in data transmission. Data needs to be downloaded again.