MYL9 silencing inhibits proliferation and migration of lung adenocarcinoma cells: a potential therapeutic target.
- 1Department of Thoracic Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
- 2Department of Geriatrics Respiratory Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Abstract
Myosin light chain 9 (MYL9), a regulatory light chain of myosin II, plays a crucial role in cytoskeletal dynamics and has been associated with tumor progression in multiple malignancies. However, its role in lung adenocarcinoma (LUAD) remains poorly characterized. Despite recent advances in treatment, the prognosis of LUAD patients remains poor, underscoring the need for novel therapeutic targets. Here, we systematically assessed MYL9 expression and its clinical relevance in LUAD by integrating transcriptomic data from The Cancer Genome Atlas (TCGA) and protein-level validation from the Human Protein Atlas (HPA) via immunohistochemistry. Functional investigations in H1299 cells indicated that silencing MYL9 significantly impeded cell proliferation, migration, and invasion, as corroborated by colony formation and Transwell assays. In vivo xenograft models further verified that MYL9 knockdown inhibited tumor growth and triggered apoptosis. Bioinformatic analyses, including the ESTIMATE algorithm, single-sample gene set enrichment analysis (ssGSEA), and drug sensitivity profiling, were also performed. In addition to its oncogenic impacts, bioinformatic analyses demonstrated that elevated MYL9 expression is correlated with distinct immune infiltration patterns and diminished chemosensitivity, possibly through the modulation of the tumor microenvironment. These findings suggest that MYL9 may link cytoskeletal regulation with tumor progression, immune remodeling, and treatment response in LUAD. Collectively, these findings recognize MYL9 as a novel prognostic biomarker and therapeutic target in LUAD, providing insights into its multifaceted role in tumor biology and treatment response. Further studies are warranted to validate these findings in larger clinical cohorts and to elucidate the underlying molecular mechanisms.
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BibTeX
@article{tan2026myl9,
title = {{MYL9 silencing inhibits proliferation and migration of lung adenocarcinoma cells: a potential therapeutic target.}},
author = {Xiang Tan and Yejun Chen and Minlian Nong and Mingwu Chen and Lei Dai},
journal = {Journal of thoracic disease},
year = {2026},
month = sep,
doi = {10.21037/jtd-2025-1-2774},
url = {https://europepmc.org/article/MED/42996939},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - MYL9 silencing inhibits proliferation and migration of lung adenocarcinoma cells: a potential therapeutic target.
AU - Xiang Tan
AU - Yejun Chen
AU - Minlian Nong
AU - Mingwu Chen
AU - Lei Dai
PY - 2026
DA - 2026/09/29
JO - Journal of thoracic disease
DO - 10.21037/jtd-2025-1-2774
UR - https://europepmc.org/article/MED/42996939
AB - Myosin light chain 9 (MYL9), a regulatory light chain of myosin II, plays a crucial role in cytoskeletal dynamics and has been associated with tumor progression in multiple malignancies. However, its role in lung adenocarcinoma (LUAD) remains poorly characterized. Despite recent advances in treatment, the prognosis of LUAD patients remains poor, underscoring the need for novel therapeutic targets. Here, we systematically assessed MYL9 expression and its clinical relevance in LUAD by integrating transcriptomic data from The Cancer Genome Atlas (TCGA) and protein-level validation from the Human Protein Atlas (HPA) via immunohistochemistry. Functional investigations in H1299 cells indicated that silencing MYL9 significantly impeded cell proliferation, migration, and invasion, as corroborated by colony formation and Transwell assays. In vivo xenograft models further verified that MYL9 knockdown inhibited tumor growth and triggered apoptosis. Bioinformatic analyses, including the ESTIMATE algorithm, single-sample gene set enrichment analysis (ssGSEA), and drug sensitivity profiling, were also performed. In addition to its oncogenic impacts, bioinformatic analyses demonstrated that elevated MYL9 expression is correlated with distinct immune infiltration patterns and diminished chemosensitivity, possibly through the modulation of the tumor microenvironment. These findings suggest that MYL9 may link cytoskeletal regulation with tumor progression, immune remodeling, and treatment response in LUAD. Collectively, these findings recognize MYL9 as a novel prognostic biomarker and therapeutic target in LUAD, providing insights into its multifaceted role in tumor biology and treatment response. Further studies are warranted to validate these findings in larger clinical cohorts and to elucidate the underlying molecular mechanisms.
SN - 2072-1439
SN - 2077-6624
ER -