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. 2023 Jan;22(1):100-116.
doi: 10.1080/15384101.2022.2109897. Epub 2022 Aug 10.

m6A modification-mediated BATF2 suppresses metastasis and angiogenesis of tongue squamous cell carcinoma through inhibiting VEGFA

Haojie Wen  1   2 , Jinyong Tang  1   2 , Yi Cui  1   2 , Minhua Hou  1   2 , Juan Zhou  1   2
Affiliations

m6A modification-mediated BATF2 suppresses metastasis and angiogenesis of tongue squamous cell carcinoma through inhibiting VEGFA

Haojie Wen et al. Cell Cycle. 2023 Jan.

Abstract

The aim is to explore the underlying mechanism of basic leucine zipper ATF-like transcription factor 2 (BATF2) in tongue squamous cell carcinoma (TSCC). The expression of BATF2 in TSCC tissues and corresponding adjacent normal TSCC tissues, human TSCC cell lines (SCC-15 and CAL-27) and human normal tongue epithelial cells NTEC was detected. Then, SCC-15 cells with stable BATF2 knockdown and CAL-27 cells with BATF2 overexpression were established to investigate the functional effect of BATF2 on TSCC. Thereafter, the effect of BATF2 on TSCC angiogenesis and BATF2 m6A methylation was also examined. BATF2 was significantly downregulated in TSCC tissues and cell lines, and BATF2 overexpression could suppress growth, metastasis and angiogenesis of TSCC. Mechanistically, vascular endothelial growth factor A (VEGFA) was identified as a downstream gene of BATF2, and it was confirmed that BATF2 suppressed growth, metastasis and angiogenesis of TSCC via inhibiting VEGFA. In addition, the N6-methyladenosine (m6A) modification of BATF2 mRNA mediated by METTL14 suppressed its expression in TSCC. METTL14/BATF2 axis could serve as a novel promising therapeutic candidate against angiogenesis for TSCC.

Keywords: BATF2; Tongue squamous cell carcinoma; VEGFA; angiogenesis; cell metastasis; m6A.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Low BATF2 expression in TSCC tissues and cells.
Figure 2.
Figure 2.
Effect of BATF2 on TSCC cell proliferation, migration and invasion.
Figure 3.
Figure 3.
Effect of BATF2 on TSCC angiogenesis.
Figure 4.
Figure 4.
VEGFA mediates the role of BATF2 in TSCC angiogenesis.
Figure 5.
Figure 5.
METTL14 inhibits BATF2 expression in TSCC via m6a modification.
Figure 6.
Figure 6.
METTL14 acts as an oncogene in TSCC through promoting m6a modification of BATF2 mRNA.
Figure 7.
Figure 7.
METTL14 induced TSCC angiogenesis via modulation of BATF2.
Figure 8.
Figure 8.
Effect of BATF2 on TSCC cell growth and metastasis in vivo.
See this image and copyright information in PMC

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References

    1. Siegel R, Miller K, Jemal A.. Cancer statistics, 2020. CA Cancer J Clin. 2020;70(1):7–30. - PubMed
    1. Zhang J, Wang L, Xie X. RFC4 promotes the progression and growth of Oral Tongue squamous cell carcinoma in vivo and vitro. J Clin Lab Anal. 2021;35(5):e23761. - PMC - PubMed
    1. Irimie A, Ciocan C, Gulei D, et al. Current insights into oral cancer epigenetics. Int J Mol Sci. 2018;19(3):670. DOI:10.3390/ijms19030670 - DOI - PMC - PubMed
    1. Zeng S, Yang J, Zhao J, et al. Silencing Dicer expression enhances cellular proliferative and invasive capacities in human tongue squamous cell carcinoma. Oncol Rep. 2014;31(2):867–873. DOI:10.3892/or.2013.2903 - DOI - PubMed
    1. Yu Z, Zhong L, Ji T, et al. MicroRNas contribute to the chemoresistance of cisplatin in tongue squamous cell carcinoma lines. Oral Oncol. 2010;46(4):317–322. DOI:10.1016/j.oraloncology.2010.02.002 - DOI - PubMed

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