CISD2 Promotes Proliferation of Colorectal Cancer Cells by Inhibiting Autophagy in a Wnt/β-Catenin-Signaling-Dependent Pathway
The aim of this study is to investigate the role of CDGSH iron-sulfur domain 2 (CISD2) in colorectal cancer (CRC). The purpose of this study was to investigate the role of CDGSH iron-sulfur domain 2 (CISD2) in colorectal cancer (CRC) progression. The expression of CISD2 in CRC cell lines was measure...
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Published in: | Biochemical genetics Vol. 61; no. 2; pp. 615 - 627 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
New York
Springer US
01-04-2023
Springer Nature B.V |
Subjects: | |
Online Access: | Get full text |
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Summary: | The aim of this study is to investigate the role of CDGSH iron-sulfur domain 2 (CISD2) in colorectal cancer (CRC). The purpose of this study was to investigate the role of CDGSH iron-sulfur domain 2 (CISD2) in colorectal cancer (CRC) progression. The expression of CISD2 in CRC cell lines was measured by western blotting. Functional assays including MTT assays and colony formation assays were performed to explore the role of CISD2 in regulating tumor growth. Flow cytometry analysis was used to examine the percentage of apoptotic CRC cells. Expression of apoptosis-related gene, autophagy-related markers, and the protein included in Wnt/β-Catenin signaling was also determined by western blotting. The in vivo role of CISD2 was also examined in a xenograft model. CISD2 expression was significantly increased in CRC cells. CISD2 promoted the CRC cell proliferation and inhibited the apoptosis and autophagy of CRC cells. Moreover, knockdown of CISD2 inhibited the activation of Wnt/β-Catenin-signaling pathway. Knockdown of CISD2 inhibited the tumor growth in nude mice. CISD2 promoted colorectal cancer development by inhibiting CRC cell apoptosis and autophagy depending on activating Wnt/β-Catenin-signaling pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-2928 1573-4927 |
DOI: | 10.1007/s10528-022-10267-8 |