E2F1 modulates RCCD1 expression to participate in the initiation and progression of EMT in colorectal cancer
Metastases in the advanced stages of colorectal cancer (CRC) present a major challenge to its treatment. Epithelial-Mesenchymal Transition (EMT) plays a crucial role in enhancing the metastasis and invasion ability of cancer cells. However, the progress of E2F transcription factor 1 (E2F1) and Regul...
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Published in | Pathology, research and practice Vol. 260; p. 155429 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Germany
Elsevier GmbH
01.08.2024
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Subjects | |
Online Access | Get full text |
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Summary: | Metastases in the advanced stages of colorectal cancer (CRC) present a major challenge to its treatment. Epithelial-Mesenchymal Transition (EMT) plays a crucial role in enhancing the metastasis and invasion ability of cancer cells. However, the progress of E2F transcription factor 1 (E2F1) and Regulator of chromatin condensation 1 (RCCD1) in CRC on EMT has not been studied.
The CRC differential expression data from The Cancer Genome Atlas database were analyzed by Gene Set Enrichment Analysis to verify the difference in expression of E2F1 and RCCD1 in cancerous and para-cancerous tissues.DNA-pull down and dual luciferase experiments confirmed that E2F1 regulates RCCD1. Western-blot and q-PCR experiments confirmed that E2F1 regulates RCCD1 and participates in the EMT-related progress of CRC.EDU, Wound healing and Transwell experiments verified the effects of regulation of E2F1 and RCCD1 on the proliferation, migration and invasion of CRC cells.
E2F1 and RCCD1 are highly expressed in cancer tissues and cancer cells. E2F1 binds to the upstream promoter of RCCD1 to regulate RCCD1 and affect the expression of EMT-related targets in CRC cells. It also affects the proliferation, migration and invasion of CRC cells.
E2F1 regulates the involvement of RCCD1 in CRC EMT and affects the proliferation, migration and invasion ability of CRC cells.
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0344-0338 1618-0631 1618-0631 |
DOI: | 10.1016/j.prp.2024.155429 |