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P55PIK 通过与 P53 特定 DNA 结构域的互动来调节癌细胞中 P53 依赖性的细胞凋亡
Authors Li C, Li W, Cheng X, Zhang D, Sun X, Zhou J, Zhou Y, Huang Y, Xia X, Ma Q, Su Z
Received 24 January 2020
Accepted for publication 6 May 2020
Published 8 June 2020 Volume 2020:13 Pages 5177—5190
DOI https://doi.org/10.2147/OTT.S247200
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Federico Perche
Purpose: Phosphatidylinositol 3-kinase (PI3K) plays an important role in tumorigenesis by cross-talking with several signaling pathways. p55PIK is a unique regulatory subunit of PI3K and contains an extra 24-residue N-terminal domain (N24). This study aimed to explore the interaction of p55PIK with p53 and the role of p55PIK in regulating p53-dependent apoptosis in cancer cells.
Materials and Methods: The expression of p55PIK was detected in cancer cells, and the interaction of p55PIK with p53 was examined by immunoprecipitation and pull-down assay. The expression of p53-dependent apoptosis-related genes was detected by PCR.
Results: N24 domain of p55PIK interacted with DNA-specific binding domain (DBD) of p53. The increase or decrease of p55PIK expression led to the change of the expression of p53 and p53-regulated genes in cancer cells. Moreover, N24 peptide led to the change of the expression of p53-regulated genes. Moreover, a membrane-permeable N24 peptide enhanced p53-dependent apoptosis induced by methyl methanesulfonate.
Conclusion: Our results reveal a novel mechanism that regulates p53-dependent apoptosis in cancer cells via p55PIK-p53 interaction.
Keywords: N24, p55PIK, p53, cancer, apoptosis