Thoracic cancer · 2025
Sortilin-1, Targeted by miR-146a, Regulates the Behavior of Non-Small Cell Lung Cancer.
СтатьяНазвание и аннотация: Перевод в очереди
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Lin Xi, Yan Zhi, Hai Ling, Niu Yan, Wen Jian-Xun, Zhu Hong-Zhe, Yan Cheng, Cha Su-Na, Yan Li, Zheng Wen-Qi, Zhang Man, Hu Zhi-De
Аннотация
BACKGROUND: Sortilin-1 (SORT1) has been implicated in the pathogenesis of various malignancies, but its role in non-small cell lung cancer (NSCLC) remains to be elucidated.
METHODS: Immunohistochemistry was employed to assess the expression of SORT1 in cancerous tissues compared to adjacent non-cancerous tissues. NSCLC cell lines, including A549, H1299, and PC-9, underwent treatment with miR-146a mimics or SORT1 small interfering RNA (siRNA), followed by evaluations of cell viability, migration, invasion, and apoptosis using cell counting kit-8, transwell assays, and scratch wound assays. Additionally, bioinformatic methods were employed to predict miR-146a target genes, which were subsequently validated through dual-luciferase reporter assays.
RESULTS: SORT1 was significantly elevated in NSCLC tissues compared to adjacent non-cancerous counterparts. Downregulation of SORT1 inhibited proliferation, invasion, migration of tumor cell lines and promoted apoptosis. Moreover, SORT1 was a direct target of miR-146a. MiR-146a modulated tumor cell proliferation, migration, invasion, and apoptosis by suppressing SORT1 expression.
CONCLUSION: These results suggest that miR-146a plays a critical role in the pathogenesis of NSCLC by targeting SORT1, highlighting its potential as a therapeutic target for NSCLC.
METHODS: Immunohistochemistry was employed to assess the expression of SORT1 in cancerous tissues compared to adjacent non-cancerous tissues. NSCLC cell lines, including A549, H1299, and PC-9, underwent treatment with miR-146a mimics or SORT1 small interfering RNA (siRNA), followed by evaluations of cell viability, migration, invasion, and apoptosis using cell counting kit-8, transwell assays, and scratch wound assays. Additionally, bioinformatic methods were employed to predict miR-146a target genes, which were subsequently validated through dual-luciferase reporter assays.
RESULTS: SORT1 was significantly elevated in NSCLC tissues compared to adjacent non-cancerous counterparts. Downregulation of SORT1 inhibited proliferation, invasion, migration of tumor cell lines and promoted apoptosis. Moreover, SORT1 was a direct target of miR-146a. MiR-146a modulated tumor cell proliferation, migration, invasion, and apoptosis by suppressing SORT1 expression.
CONCLUSION: These results suggest that miR-146a plays a critical role in the pathogenesis of NSCLC by targeting SORT1, highlighting its potential as a therapeutic target for NSCLC.