Related Experiment Video
Updated: Jul 11, 2025

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
MCF2L-AS1/miR-874-3p/STAT3 feedback loop contributes to lung adenocarcinoma cell growth and cisplatin resistance
Min Xu1, Jing Zheng2, Jun Wang3
1Department of Respiratory and Critical Care Medicine, the Fifth People's Hospital of Chengdu, China.
Background:
Long noncoding RNA (lncRNA) is widely acknowledged for its crucial role in the biological processes of various human cancers. MCF2L antisense RNA 1 (MCF2L-AS1) is a newly identified lncRNA, which remains unexplored in the context of cancer.
Methods:
MCF2L-AS1 expression was examined using qRT-PCR analysis. The impact of MCF2L-AS1 on LUAD cell growth was assessed through CCK-8, colony formation, EdU, caspase-3 activity, TUNEL, Western blot, and transwell assays. The interaction between miR-874-3p and MCF2L-AS1 or STAT3 was confirmed by RIP, luciferase reporter, and RNA pull-down assays.
Results:
Our study demonstrated the overexpression of MCF2L-AS1 in LUAD cells. Functionally, the silencing of MCF2L-AS1 hindered cell proliferation, migration, and invasion, while promoting cell apoptosis. Notably, the depletion of MCF2L-AS1 was associated with decreased cisplatin resistance. Mechanistically, MCF2L-AS1 was identified as an upstream gene of miR-874-3p, negatively regulating its expression. Following this, STAT3, the downstream target of miR-874-3p, was identified. Additionally, the expression of STAT3 was inversely related to miR-874-3p and positively regulated by MCF2L-AS1. A restoration assay suggested that MCF2L-AS1 promoted LUAD cell growth by sponging miR-874-3p and modulating STAT3 expression. Intriguingly, STAT3 was subsequently confirmed as a transcription factor that binds to the MCF2L-AS1 promoter, thereby enhancing its transcription.
Conclusions:
The MCF2L-AS1/miR-874-3p/STAT3 feedback loop plays a significant role in LUAD cell growth and cisplatin resistance.
More Related Videos
09:38Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
09:40Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Abnormal Proliferation
PI3K/mTOR/AKT Signaling Pathway
Treatment Resistant Cancers
Mitogens and the Cell Cycle
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...