ABSTRACT Non‐small cell lung cancer (NSCLC) is characterized by high incidence, mortality, and poor patient prognosis, with chemotherapy resistance being a common challenge. This research intends to identify key molecules involved in NSCLC and elucidate the regulatory role of the LINC01605/miR‐7111‐5p/ELK1 axis in chemotherapy resistance. LINC01605 and its downstream targets were predicted using the lncRNASNP2‐human and miRDB databases. RT‐qPCR was employed to measure the expression of LINC01605 across different NSCLC patients, and its prognostic value was assessed through ROC curve, Kaplan–Meier curve, and Cox regression. Dual‐luciferase reporter assay was conducted to verify interactions between miR‐7111‐5p and LINC01605 or ELK1. Transwell assay evaluated cell invasion capabilities, while CCK8 assay confirmed changes in chemotherapy drug sensitivity in chemotherapy‐resistant cells across different treatment groups. Elevated expression of LINC01605 was observed in NSCLC patients, correlating with reduced survival rates, and its expression was further elevated in patients with chemotherapy resistance. The upregulation of miR‐7111‐5p inhibited the proliferation and invasion of NSCLC cells induced by LINC01605. Mechanistically, LINC01605 negatively regulated miR‐7111‐5p expression while positively influencing ELK1 expression. Silencing ELK1 and upregulating miR‐7111‐5p levels reversed the chemotherapy resistance of A549 cells induced by LINC01605. By targeting the miR‐7111‐5p/ELK1 regulatory axis, LINC01605 induced chemotherapy resistance in NSCLC, highlighting its potential as a significant biomarker for NSCLC.
Zhang et al. (Fri,) studied this question.
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