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. 2022 Feb 19;41:69. doi: 10.1186/s13046-022-02285-6

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — m6A reader YTHDF3 decreases DICER1-AS1 stability of PC cells in response to glucose deprivation. A The DICER1-AS1 level was detected by qRT-PCR in BxPC-3 and PANC-1 cells under glucose starvation (Glu(-)). B Luciferase activity of BxPC-3 and PANC-1 cells transfected with pGL3 reporter vector containing DICER1-AS1 promoter was measured during normal or glucose starvation environment. C The effects of glucose starvation on the RNA half-life (t1/2) time of DICER1-AS1 in PC cells. D Online bioinformatics tools m6A2Target database (http://m6a2target.canceromics.org/#/) and m6A-Atlas database (http://180.208.58.66/m6A-Atlas/index.html) suggested that DICER1-AS1 has m6A sites and was the potential target of YTHDF3. E Boxplot showing the differential expression of YTHDF3 between PC tissues and normal tissues from the GEPIA database (http://gepia.cancer-pku.cn/index.html). F The expression correlation between YTHDF3 and DICER1-AS1 of PC tissues from the TCGA database. G Kaplan–Meier curves showing the survival of PC patients from the TCGA database with a low and high level of YTHDF3 using a log-rank test (cutoff value = 2819.87). H After knockdown or overexpression of YTHDF3, the expression of DICER1-AS1 was evaluated by qRT-PCR in BxPC-3 and PANC-1 cells. I The MeRIP‐qPCR showed the m6A modification was highly enriched within DICER1-AS1 in PC cells. J RIP assay showed the enrichment of DICER1-AS1 with YTHDF3 protein by using the anti-YTHDF3 antibody in PC cells. And the co-precipitated RNA was subjected to qRT-PCR for DICER1-AS1. K RIP assay showed the effects of YTHDF3 on the enrichment of DICER1-AS1 with YTHDF3 protein. L The MeRIP‐qPCR showed the effects of YTHDF3 on the enrichment of m6A with DICER1-AS1. M The effects of YTHDF3 on the RNA half-life (t1/2) time of DICER1-AS1 in actinomycin D-treated PC cells. N RIP assay showed the enrichment of DICER1-AS1 on YTHDF3 protein in BxPC-3 cells cultured in a normal or glucose-free medium for 48 h. O The MeRIP‐qPCR showed the m6A modification level of DICER1-AS1 in BxPC-3 cells cultured in a normal or glucose-free medium for 48 h. P RIP assay showed the enrichment of DICER1-AS1 on YTHDF3 protein in BxPC-3 cells transfected with siNC or siYTHDF3#1 in the normal or glucose-free medium. All data were presented as means ± SD of at least three independent experiments. Values are significant at ^aP < 0.05, ^bP < 0.01 and ^cP < 0.001 as indicated