METTL3 m6A-dependently promotes miR-21-5p maturation to accelerate choriocarcinoma progression via the HIF1AN-induced inactivation of the HIF1A/VEGF pathway

Ye, Kefan; Li, Lingchuan; Wu, Bao; Wang, Dongjie

doi:10.1007/s13258-022-01309-x

Cited by 7 publications

(7 citation statements)

References 47 publications

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“…30 METTL3 accelerated CCA cell motility by m6A-dependently promoting miR-21-5p generation. 31 Our results showed a high METTL3 expression in CCA samples and CCA cells. METTL3 overexpression promoted miR-935 and inhibited pri-miR-935 expression in CCA cells.…”

Section: Discussionsupporting

confidence: 50%

“…For example, METTL3 promoted the proliferative ability of bladder cancer cells via m6A‐dependently accelerating pri‐miR221/222 maturation 30 . METTL3 accelerated CCA cell motility by m6A‐dependently promoting miR‐21‐5p generation 31 . Our results showed a high METTL3 expression in CCA samples and CCA cells.…”

Section: Discussionmentioning

confidence: 52%

“…Gap junction A1 (GJA1, also named Cx43) maps to 6q22. 31 and belongs to the Gap junction family, which determines cellular phenotypes. 15 GJA1 is mainly expressed in epithelial tissues and can inhibit neoplasm formation by facilitating the transmission of cAMP through gap junctional intercellular communication.…”

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confidence: 99%

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METTL3 promotes choriocarcinoma progression by activating the miR‐935/GJA1 pathway in an m6A‐dependent manner

Wang,

Shi,

Zheng

2023

American J Rep Immunol

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The emerging role of microRNA‐935 (miR‐935) in modulating cancer progression has been recognized. However, its role in regulating choriocarcinoma (CCA) development and progression remains unknown. The present work aims to reveal the effect of miR‐935 on CCA cell tumor properties and the related mechanism. The RNA expression of methyltransferase 3, N6‐adenosine‐methyltransferase complex catalytic subunit (METTL3), miR‐935, and gap junction protein alpha 1 (GJA1) was detected by quantitative real‐time polymerase chain reaction. Protein expression of GJA1, Ki67, and METTL3 was measured by western blotting and immunohistochemistry assays. CCK‐8 and colony formation were used to analyze cell proliferation. Transwell assays were performed to assess cell migration and invasion. Angiogenesis was investigated by tube formation assay. Xenograft mouse model assay was used to determine miR‐935‐mediated effect on tumor formation in vivo. The luciferase reporter assay and RNA pull‐down assay were used to verify the relationship between miR‐935 and GJA1. MeRIP assay was used to analyze the m6A methylation of pri‐miR‐935. MiR‐935 expression was significantly upregulated in CCA tissues and cells when compared with control groups. MiR‐935 overexpression promoted CCA cell proliferation, migration, invasion, and tube formation and tumor tumorigenesis in vitro and in vivo, but miR‐935 knockdown showed the opposite effects. In addition, miR‐935 targeted GJA1 and mediated CCA cell tumor properties by negatively regulating GJA1 expression. METTL3 promoted miR‐935 maturation by inducing m6A methylation of pri‐miR‐935, and its overexpression contributed to CCA cell tumor properties through the regulation of miR‐935. METTL3 promoted choriocarcinoma progression by m6A‐dependently activating the miR‐935/GJA1 pathway.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 52%

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METTL3 promotes choriocarcinoma progression by activating the miR‐935/GJA1 pathway in an m6A‐dependent manner

Wang,

Shi,

Zheng

2023

American J Rep Immunol

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“…Pri-Let7a is a miRNA whose biogenesis our lab has found to be regulated by coilin ( Logan et al, 2020 ; Lett et al, 2021 ) and pri-miR-21 is a novel miRNA whose coilin-mediated biogenesis is being investigated for the first time. Both miRNAs have been previously described as being regulated by m 6 A modification ( Konno et al, 2019 ; Ye et al, 2022 ). Additionally, meRIP assays were conducted in both HeLa cells, a cancer cell line, and WI38 cells, a primary cell line.…”

Section: Resultsmentioning

confidence: 99%

Coilin mediates m6A RNA methylation through phosphorylation of METTL3

McLaurin,

Tucker,

Hebert

2023

Biology Open

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MicroRNAs (miRNAs) are a class of noncoding RNAs that regulate gene expression. An important step in miRNA biogenesis occurs when primary miRNAs are bound and cleaved by the microprocessor to generate precursor miRNAs. Regulation at this step is essential and one such regulator includes m6A RNA methylation, an RNA modification found on primary miRNAs that is installed by METTL3 and bound by hnRNPA2B1. Our lab has recently discovered that the Cajal body marker protein coilin also participates in miRNA biogenesis and hypothesized that coilin may be influencing miRNA biogenesis through m6A RNA methylation. Here we report that coilin suppression reduces m6A on primary Let7a and miR-21. We also found that coilin suppression reduced the protein expression of hnRNPA2B1 and METTL3. We observed an interaction between coilin and ectopically expressed METTL3 and found that coilin suppression reduced the nucleoplasmic portion of METTL3 and blunted ectopic METTL3 phosphorylation. Finally, coilin suppression disrupted the greater METTL3 complex with cofactors METTL14 and WTAP. Collectively, our work has uncovered a role for coilin in mediating m6A RNA methylation and provides an avenue by which coilin participates in miRNA biogenesis.

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“…activity of hif1α(Ietta et al 2006;Lee et al 2020;Ye et al 2022). It controls the transcriptional activity of hypoxia-inducible factors by hydroxylating a speci c asparagine residue (Asn-803) of the c-terminal transactivation domain of hif1α.…”

mentioning

confidence: 99%

Molecular characterization and function of hif1a and fih1 in response to acute thermal stress in American shad (Alosa sapidissima)

Liang,

Hu,

Dong

et al. 2023

Preprint

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In order to evaluate the function of hypoxia-inducible factor-1 alpha (hif1α) and factor inhibiting hif1α (fih1) in response to thermal stress, we firstly conducted functional analysis of A. sapidissima hif1α and fih1, and determined hif1α and fih1 expressions in different tissues in response to thermal stress based on identified housekeeping genes (HKGs). The results showed hif1α and fih1 were mainly located in the nucleus and cytoplasm. The full length cDNA sequence of hif1α and fih1 was 4073 bp and 2759 bp, respectively. The cDNA sequence of hif1α includes 15 exons encoding 750 amino acid residues and the full length cDNA sequence of fih1 contains 9 exons encoding 354 amino acid residues. During the acute thermal stress transferring from 16±0.5 oC (control) to 20±0.5 oC, 25±0.5 oC, and 30±0.5 oC for 15 min, it was found that the expression trends of hif1α and fih1 showed an inhibitory regulation in the heart, while they consistently expressed in other tissues. In conclusion, this is the first study to identify the tissue-specific HKGs in A. sapidissima and found that ef1α and β-actin are the most suitable HKGs. Hif1α and Fih1 is mainly the nuclear protein and cytoplasmic protein, respectively, both having high level in the heart and brain. Alosa sapidissima countered a temperature increasing from 16 ℃ to 25 ℃ by regulating the expressions of hif1α and fih1, but its physiological regulatory function was unable to cope with acute thermal stress at a temperature difference of 14 ℃ (from 16 ℃ to 30 ℃).

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METTL3 m6A-dependently promotes miR-21-5p maturation to accelerate choriocarcinoma progression via the HIF1AN-induced inactivation of the HIF1A/VEGF pathway

Cited by 7 publications

References 47 publications

METTL3 promotes choriocarcinoma progression by activating the miR‐935/GJA1 pathway in an m6A‐dependent manner

METTL3 promotes choriocarcinoma progression by activating the miR‐935/GJA1 pathway in an m6A‐dependent manner

Coilin mediates m6A RNA methylation through phosphorylation of METTL3

Molecular characterization and function of hif1a and fih1 in response to acute thermal stress in American shad (Alosa sapidissima)

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