Department of Thoracic Surgery, Ningbo First Hospital, Ningbo, China.
Department of Thoracic Surgery, The Affiliated Hospital of Medical School, Ningbo University, Ningbo, China.
J Clin Lab Anal. 2022 Oct;36(10):e24644. doi: 10.1002/jcla.24644. Epub 2022 Aug 21.
Recent literature have indicated that the malignancy of cancer cells is modulated by hsa_circ_0000423 (named circPPP1R12A) through the way of translating protein. Herein, we investigated the role and latent mechanisms of circPPP1R12A in Non-Small Cell Lung Cancer (NSCLC).
CircPPP1R12A expression was measured by qRT-PCR. The malignancy of NSCLC was determined by CCK-8, TUNEL assay, Wound healing, Transwell and Western blotting assays. The underlying mechanisms of circPPP1R12A were confirmed by Western blotting and qRT-PCR assays.
CircPPP1R12A expression in NSCLC tissues was higher than that of neighboring normal tissues. CircPPP1R12A showed an upregulated expression in NSCLC cells. Upregulation of circPPP1R12A could promote the cell viability of NSCLC cells and reduce the apoptosis of NSCLC cells, while it could not promote cell invasion and migration. The reduction of cell viability and apoptosis was discovered in NSCLC cells with the silencing of circPPP1R12A, but circPPP1R12A knockdown does not inhibit cell invasion and migration. There was something interesting that circPPP1R12A encoding protein circPPP1R12A-73aa was found in NSCLC cells. Mutations in circPPP1R12a-73AA might disrupt the function of circPPP1ra-73AA in A549 and H1299 cells. Next, we found that circPPP1R12A caused the increased growth of NSCLC cells by activating AKT signaling pathway.
In summary, our study proved that NSCLC cell proliferation was promoted by circPPP1R12A-73aa translated from circPPP1R12A through the AKT pathway, which could throw some light on the understanding of the mechanism of NSCLC.
最近的文献表明，hsa_circ_0000423（命名为 circPPP1R12A）通过翻译蛋白质的方式调节癌细胞的恶性程度。在此，我们研究了 circPPP1R12A 在非小细胞肺癌（NSCLC）中的作用和潜在机制。
通过 qRT-PCR 测量 circPPP1R12A 的表达。通过 CCK-8、TUNEL 测定、划痕愈合、Transwell 和 Western blot 测定来确定 NSCLC 的恶性程度。通过 Western blot 和 qRT-PCR 测定来验证 circPPP1R12A 的潜在机制。
NSCLC 组织中的 circPPP1R12A 表达高于相邻正常组织。circPPP1R12A 在 NSCLC 细胞中呈上调表达。circPPP1R12A 的上调可促进 NSCLC 细胞的细胞活力并减少 NSCLC 细胞的凋亡，而不会促进细胞侵袭和迁移。沉默 circPPP1R12A 可发现 NSCLC 细胞的细胞活力和凋亡减少，但 circPPP1R12A 敲低不会抑制细胞侵袭和迁移。有趣的是，在 NSCLC 细胞中发现了编码蛋白 circPPP1R12A-73aa 的 circPPP1R12A。circPPP1R12a-73AA 的突变可能会破坏 circPPP1ra-73AA 在 A549 和 H1299 细胞中的功能。接下来，我们发现 circPPP1R12A 通过激活 AKT 信号通路导致 NSCLC 细胞生长增加。
总之，我们的研究证明，circPPP1R12A-73aa 通过 AKT 通路从 circPPP1R12A 翻译，促进了 NSCLC 细胞的增殖，这为理解 NSCLC 的机制提供了一些启示。
