MiR-410-3p activates the NF-κB pathway by targeting ZCCHC10 to promote migration, invasion and EMT of colorectal cancer
| Autor: | Zeng-Hui Ma, Pei-Dong Shi, Bo-Shun Wan |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Epithelial-Mesenchymal Transition Colorectal cancer Immunology medicine.disease_cause Biochemistry Cell Line 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Western blot Cell Movement Cell Line Tumor medicine Humans Immunology and Allergy Neoplasm Invasiveness Molecular Biology Cell Proliferation Gene knockdown Reporter gene medicine.diagnostic_test NF-kappa B Zinc Fingers NF-κB Cell migration Hematology HCT116 Cells medicine.disease digestive system diseases Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology chemistry 030220 oncology & carcinogenesis Cancer research Signal transduction Colorectal Neoplasms Carcinogenesis HT29 Cells Signal Transduction |
| Zdroj: | Cytokine. 140:155433 |
| ISSN: | 1043-4666 |
| Popis: | Background Colorectal cancer (CRC) is a prevalent malignancy of the digestive tract. miR-410-3p is involved in oncogenesis and development of CRC, but the specific regulation mechanism is still not known clearly. Methods The expression of miR-410-3p and zinc finger CCHC-type containing 10 (ZCCHC10) in CRC cells was detected by qRT-PCR and western blot method, respectively. The dual-luciferase reporter gene detection was applied for determination of interaction between miR-410-3p and ZCCHC10. The wound healing assay and transwell assay were carried out to measure cell migration and invasive ability, respectively. Results The miR-410-3p expression levels were markedly increased, but ZCCHC10 levels were reduced in CRC cells and tissues. Dual-luciferase reporter gene detection indicated that miR-410-3p targeted ZCCHC10 directly. Functionally knockdown of ZCCHC10 or overexpression of miR-410-3p activated nuclear factor-κB (NF-κB) signaling pathway, promoted epithelial-mesenchymal transition (EMT) process, as well as cell migration and invasion of CRC cells. After adding NF-κB inhibitor BAY 11-708 to inhibit NF-κB pathway, the promoting effects of si-ZCCHC10 on cell migration, invasion and EMT of HT29 and SW480 cells were suppressed. Meanwhile, overexpression of ZCCHC10 inhibited the effects of miR-410-3p on cell migration, invasion and EMT of HT29 and SW480. Conclusion miR-410-3p-mediated ZCCHC10 suppression regulates NF-κB activation, thereby promoting EMT process, cell migration and invasion of CRC cells. This study provides a new insight into the specific mechanism by which miR-410-3p mediates CRC progression. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect