Fig. 3: YTHDC1 promoted the nuclear export of lnc668 by facilitating METTL3-mediated m6A modification.
a RNA-FISH experiments were conducted to measure the expression levels and nuclear-cytoplasmic distribution of lnc668 in MRC-5 cells. lnc668 primarily localized in the nuclei, with minimal expression in the cytoplasm. Under the action of TGF-β1, the expression of lnc668 increased in the nucleus and cytoplasm. However, its increase in the nucleus was less pronounced than that in the cytoplasm. Silencing METTL3 and YTHDC1 led to a reduction in the expression of lnc668 in the nucleus and cytoplasm, with a more pronounced decrease in the cytoplasm than in the nucleus. DAPI (blue) was used to stain nuclei. b Nuclear–cytoplasmic separation experiments revealed that in the normal group, lnc668 was primarily expressed in the nucleus. After TGF-β1 stimulation, lnc668 expression decreased in the nucleus and increased in the cytoplasm. Interference with METTL3 and YTHDC1 decreased cytoplasmic lnc668 expression and increased nuclear lnc668 expression. c Nuclear–cytoplasmic fractionation rescue experiments showed that in the METTL3 overexpression group, the expression of lnc668 decreased in the nucleus and increased in the cytoplasm. si-YTHDC1 reduced lnc668 expression in the cytoplasm and increased that in the nucleus, which reversed the effect of METTL3 overexpression on lnc668 in the cytoplasm and nucleus. d RNA-FISH experiments demonstrated that the lnc668 expression increased in the nucleus and cytoplasm under METTL3 overexpression, with a more pronounced increase in the cytoplasm than in the nucleus. After YTHDC1 was silenced, lnc668 expression decreased in the cytoplasm and increased in the nucleus.
