Reports of Biochemistry
and Molecular Biology
Wed, Feb 4, 2026
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Vol.14 No.2 Jul
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Yanbian University Hospital, Yanji, Jilin, 133000, China & Key Laboratory of Pathobiology of High Frequency Oncology in Ethnic Minority Areas, Yanbian University, State Ethnic Affairs Commission, Yanji, China.
Abstract: (39 Views)
Background: The relationship between non-structural maintenance of chromosomes condensin I complex subunit D2 (NCAPD2) and pancreatic cancer (PC) has never been explored, but NCAPD2 has been confirmed to play a role in a variety of tumors. This study aimed to study the anti-cancer effect of NCAPD2 in pancreatic cancer PaTu8988 cells in vitro and its mechanism.
Methods: NCAPD2 expression level within PC and the survival rate of patients was analyzed by making use the public database for bioinformatics analysis. Western blotting served to detect the expression level and knockdown level of NCAPD2 mRNA within PC. Cell Counting Kit-8 (CCK-8), colony formation, wound healing assays and Transwell assays were employed to examine the proliferation inhibition which induced by NCAPD2 knockdown. Furthermore, Western blotting was applied to analyze the influence of NCAPD2 knockdown on the p53 signaling pathway.
Results: NCAPD2 was upregulated in PC cells lines PaTu8988T and tissues and was involved in poor prognosis (P < 0.05). Down-regulation of NCAPD2 expression can effectively inhibited the proliferation, migration, and invasion processes of PC cells. Additionally, the expression levels of p53, phosphorylated p53 (p-p53), and p21 proteins were markedly reduced following NCAPD2 knockdown (P < 0.05).
Conclusion: NCAPD2 is highly expressed in PC and has poor prognosis. Its regulatory function in PC progression may be mediated through modulation of the p53 signaling pathway, thereby influencing, proliferation, apoptosis, and invasion in PaTu8988T cells.
Methods: NCAPD2 expression level within PC and the survival rate of patients was analyzed by making use the public database for bioinformatics analysis. Western blotting served to detect the expression level and knockdown level of NCAPD2 mRNA within PC. Cell Counting Kit-8 (CCK-8), colony formation, wound healing assays and Transwell assays were employed to examine the proliferation inhibition which induced by NCAPD2 knockdown. Furthermore, Western blotting was applied to analyze the influence of NCAPD2 knockdown on the p53 signaling pathway.
Results: NCAPD2 was upregulated in PC cells lines PaTu8988T and tissues and was involved in poor prognosis (P < 0.05). Down-regulation of NCAPD2 expression can effectively inhibited the proliferation, migration, and invasion processes of PC cells. Additionally, the expression levels of p53, phosphorylated p53 (p-p53), and p21 proteins were markedly reduced following NCAPD2 knockdown (P < 0.05).
Conclusion: NCAPD2 is highly expressed in PC and has poor prognosis. Its regulatory function in PC progression may be mediated through modulation of the p53 signaling pathway, thereby influencing, proliferation, apoptosis, and invasion in PaTu8988T cells.
Keywords: Cell Cycle Proteins, Non-SMC Condensin I Complex Subunit D2, Pancreatic Neoplasms, Tumor Suppressor Protein p53.
Type of Article: Original Article |
Subject:
Molecular Biology
Received: 2025/06/10 | Accepted: 2025/12/25
Received: 2025/06/10 | Accepted: 2025/12/25
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