Automated Author ProfileLai, Jie
Lai, Jie
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets for this author
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the author's datasets
Total Mentions
Total mentions of the author's datasets
S-Index Interpretation
The S-Index (Sharing Index) is a comprehensive metric that represents the cumulative impact of all your datasets. It is calculated as the sum of Dataset Index scores across all your claimed datasets.
What it means:
- A higher S-index indicates greater overall impact of your datasets relative to typical datasets in their fields of research
- The S-Index grows as you add more datasets or as existing datasets gain more citations and mentions
- It provides a single number to track your research data impact over time
Current S-Index: 0.8 (sum of 3 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
N6 methyladenosine (m6A), methylation at the sixth N atom of adenosine, is the most common and abundant modification in mammalian mRNAs and non-coding RNAs. Increasing evidence shows that the alteration of m6A modification level could regulate tumour proliferation, metastasis, self-renewal, and immune infiltration by regulating the related expression of tumour genes. However, the role of m6A modification in colorectal cancer (CRC) drug resistance is unclear. Here, MeRIP-seq and RNA-seq techniques were utilized to obtain mRNA, lncRNA expression, and their methylation profiles in 5-Fluorouracil (5-FU)-resistant colon cancer HCT-15 cells and control cells. In addition, we performed detailed bioinformatics analysis as well as in vitro experiments of lncRNA to explore the function of lncRNA with differential m6A in CRC progression and drug resistance. In this study, we obtained the m6A methylomic landscape of CRC cells and resistance group cells by MeRIP-seq and RNA-seq. We identified 3698 differential m6A peaks, of which 2224 were hypermethylated, and 1474 were hypomethylated. Among the lncRNAs, 60 were hypermethylated, and 38 were hypomethylated. GO and KEGG analysis annotations showed significant enrichment of endocytosis and MAPK signalling pathways. Moreover, knockdown of lncRNA ADIRF-AS1 and AL139035.1 promoted CRC proliferation and invasive metastasis in vitro. lncRNA- mRNA network showed that ADIRF-AS1 and AL139035.1 May play a key role in regulating drug resistance formation. We provide the first m6A methylation profile in 5-FU resistance CRC cells and analyse the functions of differential m6A-modified mRNAs and lncRNAs. Our results indicated that differential m6A RNAs were significantly associated with MAPK signalling and endocytosis after induction of 5-FU resistance. Knockdown of LncRNA ADIRF-AS1 and AL139035.1 promotes CRC progression and might be critical in regulating drug resistance formation. We outline the first m6A methylation profile of mRNA and lncRNA in CRC cells involved in 5-FU resistance.This study sought to identify the critical genes that produced 5-FU resistance by analysing the functions of differentially m6A-modified mRNAs and lncRNAs. We outline the first m6A methylation profile of mRNA and lncRNA in CRC cells involved in 5-FU resistance. This study sought to identify the critical genes that produced 5-FU resistance by analysing the functions of differentially m6A-modified mRNAs and lncRNAs.
Authors
- Lai, Jie ;
- Zhou, Zhiyong ;
- Hu, Kan ;
- Yu, HongLong ;
- Su, Xingyao ;
- Niu, Xiaoqiang ;
- Li, Huizi ;
- Mao, Shengxun
N6 methyladenosine (m6A), methylation at the sixth N atom of adenosine, is the most common and abundant modification in mammalian mRNAs and non-coding RNAs. Increasing evidence shows that the alteration of m6A modification level could regulate tumour proliferation, metastasis, self-renewal, and immune infiltration by regulating the related expression of tumour genes. However, the role of m6A modification in colorectal cancer (CRC) drug resistance is unclear. Here, MeRIP-seq and RNA-seq techniques were utilized to obtain mRNA, lncRNA expression, and their methylation profiles in 5-Fluorouracil (5-FU)-resistant colon cancer HCT-15 cells and control cells. In addition, we performed detailed bioinformatics analysis as well as in vitro experiments of lncRNA to explore the function of lncRNA with differential m6A in CRC progression and drug resistance. In this study, we obtained the m6A methylomic landscape of CRC cells and resistance group cells by MeRIP-seq and RNA-seq. We identified 3698 differential m6A peaks, of which 2224 were hypermethylated, and 1474 were hypomethylated. Among the lncRNAs, 60 were hypermethylated, and 38 were hypomethylated. GO and KEGG analysis annotations showed significant enrichment of endocytosis and MAPK signalling pathways. Moreover, knockdown of lncRNA ADIRF-AS1 and AL139035.1 promoted CRC proliferation and invasive metastasis in vitro. lncRNA- mRNA network showed that ADIRF-AS1 and AL139035.1 May play a key role in regulating drug resistance formation. We provide the first m6A methylation profile in 5-FU resistance CRC cells and analyse the functions of differential m6A-modified mRNAs and lncRNAs. Our results indicated that differential m6A RNAs were significantly associated with MAPK signalling and endocytosis after induction of 5-FU resistance. Knockdown of LncRNA ADIRF-AS1 and AL139035.1 promotes CRC progression and might be critical in regulating drug resistance formation. We outline the first m6A methylation profile of mRNA and lncRNA in CRC cells involved in 5-FU resistance.This study sought to identify the critical genes that produced 5-FU resistance by analysing the functions of differentially m6A-modified mRNAs and lncRNAs. We outline the first m6A methylation profile of mRNA and lncRNA in CRC cells involved in 5-FU resistance. This study sought to identify the critical genes that produced 5-FU resistance by analysing the functions of differentially m6A-modified mRNAs and lncRNAs.
Authors
- Lai, Jie ;
- Zhou, Zhiyong ;
- Hu, Kan ;
- Yu, HongLong ;
- Su, Xingyao ;
- Niu, Xiaoqiang ;
- Li, Huizi ;
- Mao, Shengxun
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Authors
- Lai, Jie ;
- Han, Yang ;
- Li, Hong-Mei ;
- Wang, Jia ;
- Wang, Chun-Ling ;
- Suo, Lin ;
- Sun, Ying ;
- Wang, Kai-Liang