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Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2

  • Authors:
    • Bang-Hua Zhong
    • Yu-Teng Ma
    • Jian Sun
    • Jing-Tong Tang
    • Ming Dong
  • View Affiliations / Copyright

    Affiliations: Department of Gastrointestinal Surgery, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China
    Copyright: © Zhong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 93
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    Published online on: June 4, 2024
       https://doi.org/10.3892/or.2024.8752
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Abstract

Pancreatic cancer (PC) is a malignant tumor possessing high mortality. The role of transcription factor Forkhead Box F2 (FOXF2) in PC remains unverified. The current study investigated the roles of FOXF2 in developing PC in vitro and in vivo. A xenograft tumor model was constructed with nude mice injected using FOXF2‑overexpressing PC cells or FOXF2‑silenced PC cells. High FOXF2 expression significantly enhanced the proliferation ability of PC cells in vitro and pancreatic tumor growth in vivo. The cell cycle analysis indicated that transition of G1‑S phase was promoted by FOXF2. The cell cycle‑associated proteins cyclin D1, CDK2, phosphorylated (p)‑CDK2 and p‑RB were upregulated in the FOXF2‑overexpressing cells and downregulated in the cells with FOXF2 knockdown. Flow cytometric analysis and Hoechst staining showed that the percentage of apoptotic cells was significantly increased after FOXF2 was silenced. FOXF2 knockdown promoted expression of pro‑apoptotic proteins (Bad, Bax and cleaved caspase‑3) while suppressing the anti‑apoptotic proteins (Bcl‑2 and Bcl‑xl) at the protein level. FOXF2 improved the migration and invasion of PC cells in vitro. Moreover, luciferase and chromatin immunoprecipitation assays revealed that FOXF2 binds to the MSI2 promoter, promoting its transcriptional expression. FOXF2 knockdown inhibited the MSI2 protein translation while enhancing the translation of NUMB protein, suppressing PC development in vivo. MSI2 silencing reversed the promotive effect mediated by FOXF2 on cell proliferation. These results demonstrated that FOXF2 is essential in PC progression, and the potential mechanism includes regulating MSI2 transcription.
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Copy and paste a formatted citation
Spandidos Publications style
Zhong B, Ma Y, Sun J, Tang J and Dong M: Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2. Oncol Rep 52: 93, 2024.
APA
Zhong, B., Ma, Y., Sun, J., Tang, J., & Dong, M. (2024). Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2. Oncology Reports, 52, 93. https://doi.org/10.3892/or.2024.8752
MLA
Zhong, B., Ma, Y., Sun, J., Tang, J., Dong, M."Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2". Oncology Reports 52.1 (2024): 93.
Chicago
Zhong, B., Ma, Y., Sun, J., Tang, J., Dong, M."Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2". Oncology Reports 52, no. 1 (2024): 93. https://doi.org/10.3892/or.2024.8752
Copy and paste a formatted citation
x
Spandidos Publications style
Zhong B, Ma Y, Sun J, Tang J and Dong M: Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2. Oncol Rep 52: 93, 2024.
APA
Zhong, B., Ma, Y., Sun, J., Tang, J., & Dong, M. (2024). Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2. Oncology Reports, 52, 93. https://doi.org/10.3892/or.2024.8752
MLA
Zhong, B., Ma, Y., Sun, J., Tang, J., Dong, M."Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2". Oncology Reports 52.1 (2024): 93.
Chicago
Zhong, B., Ma, Y., Sun, J., Tang, J., Dong, M."Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2". Oncology Reports 52, no. 1 (2024): 93. https://doi.org/10.3892/or.2024.8752
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