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EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells
Tingting Cai1,2, Jieqi Zhou1,2, Yuanyuan Zeng1,2,3
1Department of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Background:
The Ecotropic viral integration site 5 (EVI5), an important protein in regulating cell cycle, cytokinesis and cellular membrane traffic, functions as a stabilizing factor maintaining anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 in S/G2 phase. However, the mechanism by which EVI5 promotes malignant transformation of non-small cell lung cancer (NSCLC) remains unknown. In the present study, we addressed the role of EVI5 in NSCLC by regulating tumor growth, migration and invasion.
Methods:
The expression levels of EVI5 and miR-486-5p in NSCLC tissues and cells were measured by real-time PCR. Meanwhile, EVI5 and its associated protein expression were analyzed by western blot and co-immunoprecipitation assay. Flow cytometry was performed to determine cell proliferation and apoptosis. CCK-8 and clonogenic assays were used to analyze cell viability. Wound healing, transwell migration and matrigel invasion assays were utilized to assess the motility of tumor cells. To investigate the role of EVI5 in vivo, lung carcinoma xenograft mouse model was applied..
Results:
EVI5 was upregulated in NSCLC tissues and cell lines when compared with that in normal tissues and cell line. Knockdown of EVI5 in vitro inhibited tumor cell proliferation, migration and invasion in NSCLC cells. Further, inoculation of EVI5-deficient tumor cells into nude mice suppressed tumor proliferation and metastasis compared to control mice inoculated with unmanipulated tumor cells. These data indicated that EVI5 promote the proliferation of NSCLC cells which was consistent with our previous results. Additionally, we showed that EVI5 was directly regulated by miR-486-5p, and miR-486-5p-EVI5 axis affected the NSCLC migration and invasion through TGF-β/Smad signaling pathway by interacting with TGF-β receptor II and TGF-β receptor I.
Conclusions:
Based on these results, we demonstrated a new post-transcriptional mechanism of EVI5 regulation via miR-486-5p and the protumoral function of EVI5 in NSCLC by interacting with Emi1 and/or TGF-β receptors, which provides a new insight into the targeted therapy of NSCLC.
Insights
Ecotropic viral integration site 5 (EVI5) promotes non-small cell lung cancer (NSCLC) growth and metastasis. MiR-486-5p directly targets EVI5, offering a potential therapeutic strategy for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Ecotropic viral integration site 5 (EVI5) is crucial for cell cycle regulation and maintains anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 stability.
- The precise mechanism by which EVI5 drives non-small cell lung cancer (NSCLC) malignancy remains unclear.
- This study investigates the role of EVI5 in NSCLC tumor growth, migration, and invasion.
Purpose of the Study:
- To elucidate the role of EVI5 in NSCLC progression.
- To identify regulatory mechanisms of EVI5 in NSCLC.
- To explore EVI5 as a potential therapeutic target in NSCLC.
Main Methods:
- Quantitative real-time PCR and western blotting to assess EVI5 and miR-486-5p expression.
- Co-immunoprecipitation assays to analyze protein interactions.
- Cell proliferation, apoptosis, migration, and invasion assays (flow cytometry, CCK-8, clonogenic, wound healing, Transwell).
- In vivo studies using a lung carcinoma xenograft mouse model.
Main Results:
- EVI5 expression is significantly upregulated in NSCLC tissues and cell lines.
- EVI5 knockdown inhibits NSCLC cell proliferation, migration, and invasion in vitro and suppresses tumor growth and metastasis in vivo.
- EVI5 is directly regulated by miR-486-5p, and this axis influences NSCLC progression via the TGF-β/Smad signaling pathway.
Conclusions:
- EVI5 promotes NSCLC progression through interactions with Emi1 and TGF-β receptors.
- MiR-486-5p acts as a negative regulator of EVI5, impacting NSCLC cell behavior.
- The miR-486-5p-EVI5 pathway presents a novel therapeutic target for NSCLC treatment.
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