From: Tracing vitamins on the long non-coding lane of the transcriptome: vitamin regulation of LncRNAs
Vitamin | LncRNA(s) studied in the project | System: Patients / cell line(s) / animal model | Highlighted lncRNA(s)/pathway(s)/target(s)/ partners/ interactions | Disease context/ implication for human disease | Main result(s) | Ref |
---|---|---|---|---|---|---|
Vitamin C | Differentially expressed mRNAs (1232) and lncRNAs (937) after treatment with ascorbic acid | Swine testicular cell line | MAPK, AMPK, PI3K-Akt and mTOR and pathways regulating cell proliferation and cell cycle | Reproduction of male animals | transcriptomic analysis demonstrated AA-induced differentially expressed mRNAs and lncRNAs enriched in MAPK, AMPK, PI3K-Akt and mTOR and pathways | [104] |
MALAT1 | Human CRC cell lines: LS174T, HT-29, and SW480 Athymic nude mice (Balb/c, nu/nu) | _ | Colorectal Cancer | Vitamin C could suppress proliferation, induce apoptosis and arrest cell cycle. More killing effects were observed in cells with high MALAT1 expression | [105] | |
RNA sequencing of donner cells before and after vitamin C treatment/ differentially expressed mRNAs and lncRNAs | Oocytes and donor fibroblasts of bovine origin | _ | improve cloned bovine embryo formation by somatic cell nuclear transfer from fibroblast donor cells | Vitamin C improved colony formation by restoring mRNA and lncRNA expression signature | [106] | |
X-inactive specific transcript (Xist) | Mouse embryonic fibroblasts (MEFs) | _ | Reprogramming of female somatic cells into induced pluripotent stem cells (iPSCs) | Vitamin C has a key role in keeping Xist repressed, reactivating the X chromosome during the pre‐iPSC to iPSC transition | [107] |