肺癌（其中肺腺癌占病例的 40% 以上）构成了全球健康挑战。有证据表明长非编码 RNA (lncRNA)，例如 GUSBP11，可能具有治疗潜力。因此我们探讨了GUSBP11在肺腺癌中的作用和机制。生物信息学分析表明，GUSBP11 在肺腺癌中表达上调，并与预后恶化相关。定量 PCR (qPCR) 分析显示，与癌旁组织样本相比，GUSBP11 在 61 对肺腺癌患者肿瘤中高表达。 GUSBP11敲低可抑制肺腺癌细胞的体外增殖和转移，同时促进细胞凋亡，而GUSBP11的沉默会损害肺腺癌的体内肿瘤生长。机制研究揭示了 GUSBP11 在抑制 KHSRP 调节功能中的作用，KHSRP 是肺腺癌细胞增殖和转移所必需的蛋白质。总而言之，我们的研究结果强调了靶向 GUSBP11-KHSRP 轴在肺腺癌中的治疗和诊断潜力，为临床环境中的进一步探索铺平了道路。

Lung cancer, with lung adenocarcinoma comprising over 40% of cases, presents a global health challenge. Evidence indicates that long non-coding RNAs (lncRNAs), such as GUSBP11, could have therapeutic potential. Thus we explored the role and mechanism of GUSBP11 in lung adenocarcinoma. Bioinformatics analyses demonstrated GUSBP11 was upregulated in lung adenocarcinoma and was correlated with worsening prognosis. Quantitative PCR (qPCR) analysis revealed that of GUSBP11 was highly expressed in 61 paired lung adenocarcinoma patient tumor compared to paracancerous tissue samples. GUSBP11 knockdown suppressed lung adenocarcinoma cells proliferation and metastasis in vitro while promoted cell apoptosis, and the silencing of GUSBP11 impaired in vivo tumor growth in lung adenocarcinoma. Mechanistic insights revealed GUSBP11's role in inhibiting the regulatory functions of KHSRP, a protein essential for lung adenocarcinoma cell proliferation and metastasis. Taken together, our findings underscore the therapeutic and diagnostic potential of targeting the GUSBP11-KHSRP axis in lung adenocarcinoma, paving the way for further exploration in clinical settings.