ArticleCytotechnology2025
Silencing of LINC01278 promotes sensitivity of non-small cell lung cancer cells to osimertinib by targeting miR-324-3p/ZFX axis.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Long Non-coding RNAs in Non-small Cell Lung Carcinoma: Regulatory Mechanisms, Diagnostic Potential, and Therapeutic Perspectives.Current drug targets · 2026Review
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5 authors.
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Abstract
Osimertinib has been demonstrated to be effective for improving the prognosis of patients with epidermal growth factor receptor mutation-positive lung cancer. However, osimertinib resistance inevitably emerges throughout the treatment course. This study explored the function and mechanism of long noncoding RNA LINC01278 in osimertinib-resistant NSCLC cells. Osimertinib-resistant non-small cell lung cancer (NSCLC) cells were established by treating PC9 and HCC827 cells with increasing doses of osimertinib for over 6 months. LINC01278 expression in parental and drug-resistant cells (PC9-OR and HCC827-OR) was measured by polymerase chain reaction. Cell counting kit 8 assays were used to examine cell viability and half-maximal inhibitory concentration values. The effects of LINC01278 knockdown on cell proliferation and apoptosis were measured by colony formation assays and flow cytometry. A luciferase reporter assay was performed to verify the interaction between LINC01278 and miR-324-3p or the binding ability between miR-324-3p and ZFX. Protein levels of ZFX and apoptotic markers in NSCLC cells were measured by western blotting. As shown by experimental results, LINC01278 was highly expressed in osimertinib-resistant NSCLC cells compared to its expression in parental cells. The silencing of LINC01278 improved the sensitivity of drug-resistant cells towards osimertinib. LINC1278 depletion inhibited osimertinib-resistant cell proliferation while promoting cell apoptosis. LINC01278 interacted with miR-324-3p to regulate ZFX expression. ZFX could be targeted by miR-324-3p in PC9-OR and HCC827-OR cells. ZFX overexpression counteracted the suppressive impact of LINC01278 silencing on the malignant behavior of PC9-OR and HCC827-OR cells. In conclusion, LINC01278 knockdown alleviates osimertinib resistance of NSCLC cells by regulating downstream miR-324-3p and ZFX. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-024-00673-8.
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