Linc-smad7 is involved in the regulation of lipid synthesis in mouse mammary epithelial cells
Copyright © 2024. Published by Elsevier B.V..
Long intergenic non-coding RNA(lincRNA) is transcribed from the intermediate regions of coding genes and plays a pivotal role in the regulation of lipid synthesis. N6-methyladenosine (m6A) modification is widely prevalent in eukaryotic mRNAs and serves as a regulatory factor in diverse biological processes. This study aims to delineate the mechanism by which Linc-smad7 mediates m6A methylation to regulate milk fat synthesis. Tissue expression analysis in this study revealed a high expression of Linc-smad7 in breast tissue during pregnancy. Cell proliferation assays, including CCK8 and EdU assays, demonstrated that Linc-smad7 had no significant impact on the proliferation of mammary epithelial cells. However, during mammary epithelial cell differentiation, the overexpression of Linc-smad7 led to reduced lipid formation, whereas interference with Linc-smad7 promoted lipogenesis. Mechanistically, Linc-smad7 was found to modulate RNA m6A levels, as evidenced by dot blot assays and methylated RNA immunoprecipitation sequencing (MeRIP-Seq). Subsequent validation through RT-qPCR corroborated these findings, aligning with the m6A sequencing outcomes. Furthermore, co-transfection experiments elucidated that Linc-smad7 regulates lipid synthesis in mammary epithelial cells by influencing the expression of METTL14. In summary, these findings underscore the regulatory role of Linc-smad7 in controlling METTL14 gene expression, thereby mediating m6A modifications to regulate lipid synthesis in mammary epithelial cells.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:262 |
|---|---|
| Enthalten in: |
International journal of biological macromolecules - 262(2024), Pt 1 vom: 21. März, Seite 129875 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Fang, Xue [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Journal Article |
|---|
| Anmerkungen: |
Date Completed 20.03.2024 Date Revised 20.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.ijbiomac.2024.129875 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM368100189 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM368100189 | ||
| 003 | DE-627 | ||
| 005 | 20240320234120.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240207s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.ijbiomac.2024.129875 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1337.xml |
| 035 | |a (DE-627)NLM368100189 | ||
| 035 | |a (NLM)38320638 | ||
| 035 | |a (PII)S0141-8130(24)00678-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Fang, Xue |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Linc-smad7 is involved in the regulation of lipid synthesis in mouse mammary epithelial cells |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 20.03.2024 | ||
| 500 | |a Date Revised 20.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2024. Published by Elsevier B.V. | ||
| 520 | |a Long intergenic non-coding RNA(lincRNA) is transcribed from the intermediate regions of coding genes and plays a pivotal role in the regulation of lipid synthesis. N6-methyladenosine (m6A) modification is widely prevalent in eukaryotic mRNAs and serves as a regulatory factor in diverse biological processes. This study aims to delineate the mechanism by which Linc-smad7 mediates m6A methylation to regulate milk fat synthesis. Tissue expression analysis in this study revealed a high expression of Linc-smad7 in breast tissue during pregnancy. Cell proliferation assays, including CCK8 and EdU assays, demonstrated that Linc-smad7 had no significant impact on the proliferation of mammary epithelial cells. However, during mammary epithelial cell differentiation, the overexpression of Linc-smad7 led to reduced lipid formation, whereas interference with Linc-smad7 promoted lipogenesis. Mechanistically, Linc-smad7 was found to modulate RNA m6A levels, as evidenced by dot blot assays and methylated RNA immunoprecipitation sequencing (MeRIP-Seq). Subsequent validation through RT-qPCR corroborated these findings, aligning with the m6A sequencing outcomes. Furthermore, co-transfection experiments elucidated that Linc-smad7 regulates lipid synthesis in mammary epithelial cells by influencing the expression of METTL14. In summary, these findings underscore the regulatory role of Linc-smad7 in controlling METTL14 gene expression, thereby mediating m6A modifications to regulate lipid synthesis in mammary epithelial cells | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Linc-smad7 | |
| 650 | 4 | |a Lipid synthesis | |
| 650 | 4 | |a Mammary epithelial cell | |
| 650 | 4 | |a N(6)-methyladenosine | |
| 650 | 7 | |a RNA, Messenger |2 NLM | |
| 650 | 7 | |a Lipids |2 NLM | |
| 700 | 1 | |a Chen, Junhao |e verfasserin |4 aut | |
| 700 | 1 | |a Meng, Fantong |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Fang |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Xi |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Yanhong |e verfasserin |4 aut | |
| 700 | 1 | |a Fang, Xingtang |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Chunlei |e verfasserin |4 aut | |
| 700 | 1 | |a Song, Chengchuang |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t International journal of biological macromolecules |d 1992 |g 262(2024), Pt 1 vom: 21. März, Seite 129875 |w (DE-627)NLM012627356 |x 1879-0003 |7 nnns |
| 773 | 1 | 8 | |g volume:262 |g year:2024 |g number:Pt 1 |g day:21 |g month:03 |g pages:129875 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.ijbiomac.2024.129875 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 262 |j 2024 |e Pt 1 |b 21 |c 03 |h 129875 | ||