RFWD3 Knockdown Inhibits Cancer Cell Proliferation, Migration, and Invasion while Promoting Apoptosis of Non-Small Cell Lung Cancer Cells

RING finger and WD repeat domain 3 (RFWD3) expression is elevated in various tumor types, but its precise role in non-small cell lung cancer (NSCLC) remains unclear. This study aims to investigate the biological function of RFWD3 in NSCLC and the associated molecular pathways. RFWD3 expression was knocked down in NSCLC cells through transfection. Cell apoptosis was analyzed using flow cytometry, cell viability was assessed using the cell counting kit-8 (CCK-8), and the migration and invasion of NSCLC cells were evaluated using Transwell chamber assays. Additionally, the expression of BAX, BCL-2, cleaved-caspase-3, and key signaling molecules involved in the ERK/p38 pathway was determined using Western blotting. The expression of RFWD3 was found to be elevated in NSCLC cells compared with normal lung epithelial BEAS-2B cells. Its knockdown led to reduced cell proliferation, migration, and invasion and increased apoptosis rate, partially through the inhibition of the ERK/p38 signaling pathway. Knockdown of the <i>RFWD3</i> gene inhibited NSCLC cell proliferation, migration, and invasion while also inducing apoptosis. These effects are partially attributed to the blockade of the ERK/p38 signaling pathway.

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Publication Details

Journal
Archivum Immunologiae et Therapiae Experimentalis
Published
2025-01-01
DOI
https://doi.org/10.2478/aite-2025-0019
Primary Topic
RNA modifications and cancer
Type
article
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article

RFWD3 Knockdown Inhibits Cancer Cell Proliferation, Migration, and Invasion while Promoting Apoptosis of Non-Small Cell Lung Cancer Cells

Ting Ma, Baolan Wang
Archivum Immunologiae et Therapiae Experimentalis
RNA modifications and cancer
article

RFWD3 Knockdown Inhibits Cancer Cell Proliferation, Migration, and Invasion while Promoting Apoptosis of Non-Small Cell Lung Cancer Cells

Ting Ma, Baolan Wang
article en

Abstract

RING finger and WD repeat domain 3 (RFWD3) expression is elevated in various tumor types, but its precise role in non-small cell lung cancer (NSCLC) remains unclear. This study aims to investigate the biological function of RFWD3 in NSCLC and the associated molecular pathways. RFWD3 expression was knocked down in NSCLC cells through transfection. Cell apoptosis was analyzed using flow cytometry, cell viability was assessed using the cell counting kit-8 (CCK-8), and the migration and invasion of NSCLC cells were evaluated using Transwell chamber assays. Additionally, the expression of BAX, BCL-2, cleaved-caspase-3, and key signaling molecules involved in the ERK/p38 pathway was determined using Western blotting. The expression of RFWD3 was found to be elevated in NSCLC cells compared with normal lung epithelial BEAS-2B cells. Its knockdown led to reduced cell proliferation, migration, and invasion and increased apoptosis rate, partially through the inhibition of the ERK/p38 signaling pathway. Knockdown of the <i>RFWD3</i> gene inhibited NSCLC cell proliferation, migration, and invasion while also inducing apoptosis. These effects are partially attributed to the blockade of the ERK/p38 signaling pathway.

Archivum Immunologiae et Therapiae ExperimentalisVol. 73(1)
Huaian First People’s Hospital (CN), Nanjing Medical University (CN)
Good health and well-being
Openalex Percentile: Top 87%
RNA modifications and cancer
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RFWD3 Knockdown Inhibits Cancer Cell Proliferation, Migration, and Invasion while Promoting Apoptosis of Non-Small Cell Lung Cancer Cells — Ting Ma, Baolan Wang · Archivum Immunologiae et Therapiae Experimentalis (2025) | TGRS Research Map | TGRS