Although MRPS16 is involved in cancer development, its mechanisms in developing LAUD remain unclear. Herein, qRT‐PCR, WB and IHC were utilized for evaluating MRPS16 expression levels, while functional assays besides animal experiments were performed to measure MRPS16 effect on LAUD progression. Using WB, the MRPS16 effect on PI3K/AKT/Frataxin signalling pathway was tested. According to our study, MRPS16 was upregulated in LAUD and was correlated to the advanced TNM stage as well as poor clinical outcomes, which represent an independent prognostic factor. Based on functional assays, MRPS16 is involved in promoting LAUD growth, migration and invasion, which was validated further in subsequent analyses through PI3K/AKT/Frataxin pathway activation. Moreover, MRPS16‐knockdown‐mediated Frataxin overexpression was shown to restore the reduction in tumour cells proliferation, migration and invasion. Our results revealed that MRPS16 caused an aggressive phenotype to LAUD and was a poor prognosticator; thus, targeting MRPS16 may be effectual in LAUD treatment.

中文翻译：

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MRPS16 通过 PI3K/AKT/Frataxin 信号轴促进肺腺癌生长

尽管 MRPS16 参与癌症发展，但其发展 LAUD 的机制仍不清楚。在此，利用qRT-PCR、WB和IHC来评估MRPS16表达水平，同时进行动物实验以外的功能测定来测量MRPS16对LAUD进展的影响。使用WB测试了MRPS16对PI3K/AKT/Frataxin信号通路的影响。根据我们的研究，MRPS16 在 LAUD 中表达上调，并且与晚期 TNM 分期以及不良临床结果相关，这代表了独立的预后因素。根据功能分析，MRPS16 参与促进 LAUD 生长、迁移和侵袭，这在后续分析中通过 PI3K/AKT/Frataxin 通路激活得到了进一步验证。此外，MRPS16 敲低介导的 Frataxin 过度表达被证明可以恢复肿瘤细胞增殖、迁移和侵袭的减少。我们的结果显示，MRPS16 导致 LAUD 具有侵袭性表型，并且是一个较差的预测因子；因此，靶向 MRPS16 可能在 LAUD 治疗中有效。