Human Pleural Mesothelioma (HPM) is an aggressive asbestos-related tumor with limited treatment options and a poor prognosis. MicroRNAs (miRNAs), known to play key roles in the pathogenesis of HPM, have emerged as promising candidates for both diagnostic and therapeutic applications. Among them, miR-197-3p has been previously identified as dysregulated in sera from HPM patients and workers ex-exposed to asbestos fibers. To investigate the functional role of miR-197-3p, loss- and gain-of-function studies were performed in HPM cell lines and human mesothelial cells (HMC) using miR-197-3p-specific antagomiR and mimic. The effects of miR-197-3p modulation on cell proliferation, viability, migration, and apoptosis were evaluated. In addition, bioinformatics analyses were performed to identify potential miR-197-3p target genes, which were subsequently evaluated at both mRNA and protein levels. MiR-197-3p tested significantly upregulated in HPM cells. Its inhibition led to a marked reduction of the HPM cell proliferation, whereas its overexpression in HMC promoted a proliferative phenotype, supporting a potential role in cell growth regulation. Among the predicted targets, TGF-β1 and p120 showed modulation at the mRNA level, although protein-level changes were limited or only partially consistent. These findings suggest that miR-197-3p may contribute to HPM pathogenesis by promoting cell proliferation and influencing critical molecular pathways. However, the underlying molecular mechanisms remain to be fully elucidated, and the interaction with candidate targets, such as TGF-β1 and p120, should be considered putative. Further investigations, including functional and mechanistic validation in more representative experimental models, will be required to clarify the role of miR-197-3p in HPM pathobiology.
Proliferation of pleural mesothelioma cells is enhanced by the microRNA-197-3p activity
Ilaria BononiCo-primo
;Giulia Di MauroCo-primo
;Maria Letizia TramarinCo-primo
;Valentina Esposito;Giulia Tonnini;Lucia Oton-Gonzalez;Beatrice Dallan;Elena Torreggiani
;Fernanda Martini
Penultimo
;Mauro Tognon
Ultimo
2026
Abstract
Human Pleural Mesothelioma (HPM) is an aggressive asbestos-related tumor with limited treatment options and a poor prognosis. MicroRNAs (miRNAs), known to play key roles in the pathogenesis of HPM, have emerged as promising candidates for both diagnostic and therapeutic applications. Among them, miR-197-3p has been previously identified as dysregulated in sera from HPM patients and workers ex-exposed to asbestos fibers. To investigate the functional role of miR-197-3p, loss- and gain-of-function studies were performed in HPM cell lines and human mesothelial cells (HMC) using miR-197-3p-specific antagomiR and mimic. The effects of miR-197-3p modulation on cell proliferation, viability, migration, and apoptosis were evaluated. In addition, bioinformatics analyses were performed to identify potential miR-197-3p target genes, which were subsequently evaluated at both mRNA and protein levels. MiR-197-3p tested significantly upregulated in HPM cells. Its inhibition led to a marked reduction of the HPM cell proliferation, whereas its overexpression in HMC promoted a proliferative phenotype, supporting a potential role in cell growth regulation. Among the predicted targets, TGF-β1 and p120 showed modulation at the mRNA level, although protein-level changes were limited or only partially consistent. These findings suggest that miR-197-3p may contribute to HPM pathogenesis by promoting cell proliferation and influencing critical molecular pathways. However, the underlying molecular mechanisms remain to be fully elucidated, and the interaction with candidate targets, such as TGF-β1 and p120, should be considered putative. Further investigations, including functional and mechanistic validation in more representative experimental models, will be required to clarify the role of miR-197-3p in HPM pathobiology.| File | Dimensione | Formato | |
|---|---|---|---|
|
Frontiers in Oncology 2026.pdf
accesso aperto
Descrizione: Frontiers in Oncology 2026
Tipologia:
Full text (versione editoriale)
Licenza:
Creative commons
Dimensione
1.71 MB
Formato
Adobe PDF
|
1.71 MB | Adobe PDF | Visualizza/Apri |
I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


