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. 2023 May 21;12(13):14440–14451. doi: 10.1002/cam4.6072

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© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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MSANTD2‐004 regulated the bladder cancer cells malignant phenotype. (A) CCK8 assay. (B) Cell clone formation. (C) Cell migration. (D) Cell invasion. (E) Cell apoptosis. (F) Graphical representation of the regulation and function of BCLET rs558814 in bladder cancer. Single nucleotide polymorphism (SNP) rs558814 A>G in BCLET was significantly associated with a reduced risk of bladder cancer. Furthermore, BCLET mediated cell proliferation, Transwell activity, and tumorigenesis to participate in bladder oncogenesis. BCLET ultimately bound MSANTD2 and increased the expression of MSANTD2‐004 by modulating alternative splicing (AS) of MSANTD2 exon 1.