Activation of CHPF by transcription factor NFIC promotes NLRP3 activation during the progression of colorectal cancer
© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature..
Given the role of chondroitin polymerizing factor (CHPF) in several cancers, we investigated its role in the progression of colorectal cancer (CRC) and its association with NLRP3 inflammasome activation. High expression of CHPF in CRC predicted poor patient prognosis. Using colony formation, EdU staining, wound healing, Transwell invasion, and flow cytometry assays, we revealed that the downregulation of CHPF inhibited the malignant behavior of CRC cells. CHPF promoted NLRP3 inflammasome activation by inducing the MAPK signaling pathway, as evidenced by enhanced expression of Phos-ERK1/2, Phos-MEK1, Phos-MEK2, and NLRP3. Additionally, nuclear factor 1 C-type (NFIC) was revealed as a potential upstream transcription factor of CHPF in the modulation of CRC, and the anti-tumor effects elicited through its knockdown were compromised by CHPF in vitro and in vivo. In summary, we demonstrated that NFIC promoted NLRP3 activation to support CRC development via the CHPF-mediated MAPK signaling.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
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| Enthalten in: |
Functional & integrative genomics - 24(2024), 1 vom: 24. Jan., Seite 20 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wu, Jiamei [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 05.02.2024 Date Revised 21.02.2024 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s10142-024-01299-x |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM367581558 |
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| 520 | |a © 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature. | ||
| 520 | |a Given the role of chondroitin polymerizing factor (CHPF) in several cancers, we investigated its role in the progression of colorectal cancer (CRC) and its association with NLRP3 inflammasome activation. High expression of CHPF in CRC predicted poor patient prognosis. Using colony formation, EdU staining, wound healing, Transwell invasion, and flow cytometry assays, we revealed that the downregulation of CHPF inhibited the malignant behavior of CRC cells. CHPF promoted NLRP3 inflammasome activation by inducing the MAPK signaling pathway, as evidenced by enhanced expression of Phos-ERK1/2, Phos-MEK1, Phos-MEK2, and NLRP3. Additionally, nuclear factor 1 C-type (NFIC) was revealed as a potential upstream transcription factor of CHPF in the modulation of CRC, and the anti-tumor effects elicited through its knockdown were compromised by CHPF in vitro and in vivo. In summary, we demonstrated that NFIC promoted NLRP3 activation to support CRC development via the CHPF-mediated MAPK signaling | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CHPF | |
| 650 | 4 | |a Colorectal cancer | |
| 650 | 4 | |a MAPK signaling pathway | |
| 650 | 4 | |a NFIC | |
| 650 | 4 | |a NLRP3 inflammasome | |
| 650 | 7 | |a Inflammasomes |2 NLM | |
| 650 | 7 | |a NFI Transcription Factors |2 NLM | |
| 650 | 7 | |a NFIC protein, human |2 NLM | |
| 650 | 7 | |a NLR Family, Pyrin Domain-Containing 3 Protein |2 NLM | |
| 650 | 7 | |a chondroitin synthase |2 NLM | |
| 650 | 7 | |a EC 2.4.1.175 |2 NLM | |
| 650 | 7 | |a NLRP3 protein, human |2 NLM | |
| 700 | 1 | |a Wang, Miao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Yuechuan |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Guohong |e verfasserin |4 aut | |
| 700 | 1 | |a Xing, Yutong |e verfasserin |4 aut | |
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