ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2026
[Effects of LINC00641 on the Malignant Progression and Chemotherapy Resistance of Non-small Cell Lung Cancer H1299 Cells by Regulating the miR-1306-5p/FGFR3 Axis].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNon-small cell lung cancer (NSCLC) is one of the causes of cancer-related deaths worldwide. Although platinum-based chemotherapy is the main treatment method for advanced patients, acquired resistance often leads to treatment failure. Long non-coding RNAs (lncRNAs) play an important role in tumor occurrence and development, but the specific mechanism of their involvement in chemotherapy resistance in NSCLC is not yet fully understood. This study aims to explore the effect of LINC00641 on the microRNA-1306-5p (miR-1306-5p)/fibroblast growth factor receptor 3 (FGFR3) axis on the malignant progression and chemotherapy resistance of NSCLC cell line H1299.
methodsThe mRNA expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR); and the interaction was verified by the dual-luciferase reporter gene assay. H1299 cells were randomly divided into the following groups: CG group (normal culture), sh-NC group (transfected with sh-NC), sh-LINC00641 group (transfected with sh-LINC00641), sh-LINC00641+anti-NC group (transfected with sh-LINC00641 and anti-NC), sh-LINC00641+anti-miR-1306-5p group (transfected with sh-LINC00641 and anti-miR-1306-5p), mimic-NC group (transfected with mimic-NC), miR-1306-5p-mimics group (transfected with miR-1306-5p-mimics), miR-1306-5p-mimics+OE-NC group (transfected with miR-1306-5p-mimics and OE-NC), and miR-1306-5p-mimics+OE-FGFR3 group (transfected with miR-1306-5p-mimics and OE-FGFR3). Then cell proliferation, migration, and invasion were measured by plate colony formation assay, scratch assay, and Transwell assay, respectively. In addition, H1299/DDP cells were grouped as mentioned above. After that, the chemotherapy resistance of H1299/DDP cells was detected by the MTT method. And Western blot was implemented to detect the protein expressions of FGFR3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 13 (MMP-13), integrin β1 in H1299 cells, and the P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1) in H1299/DDP cells.
resultsIn NSCLC tissues or cells (H1299, H1299/DDP), LINC00641 and FGFR3 were highly expressed, while miR‑1306‑5p was lowly expressed, and the expression trends of these three factors changed more significantly in the drug‑resistant cell line H1299/DDP (P<0.05). LINC00641 could negatively regulate miR‑1306‑5p in a targeted manner; and miR‑1306‑5p could negatively regulate FGFR3 in a targeted manner. Knockdown of LINC00641 (sh‑LINC00641) or overexpression of miR‑1306‑5p reduced the clone number, scratch healing rate, migration number, invasion number, and the expression of PCNA, MMP‑13, and integrin β1 proteins in H1299 cells (P<0.05), and also suppressed the optical density (OD)540 value and the expression of P‑gp and MRP1 proteins in H1299/DDP cells (P<0.05). In addition, inhibition of miR‑1306‑5p or overexpression of FGFR3 could reverse the inhibitory effects of LINC00641 knockdown or miR‑1306‑5p overexpression on the proliferation, migration, invasion, and chemoresistance of H1299 cells (P<0.05).
conclusionsKnockdown of LINC00641 can regulate the miR-1306-5p/FGFR3 axis, inhibit the malignant progression and chemotherapy resistance of NSCLC cells, and provide a new candidate target for molecular intervention of chemotherapy resistance in NSCLC.
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