结直肠癌（CRC）是一种发生在直肠或结肠的癌症，发病率很高。精子相关抗原 5 (SPAG5) 是一种调节细胞分裂的基因，已观察到在多种癌症中高表达，但其在结直肠癌中的作用尚不清楚。本研究旨在探讨SPAG5在CRC中的调节作用。通过The Cancer Genome Atlas和Tumor Immune Estimation Resource预测了SPAG5在多种癌症和正常组织中的表达，并验证了SPAG5在人正常肠上皮细胞NCM460和人CRC细胞系Caco2、HT29、SW480和LOVO中的表达通过蛋白质印迹（WB）。然后通过细胞计数试剂盒8、WB和流式细胞术研究沉默SPAG5对细胞活力、增殖和凋亡的影响。通过划痕实验和Transwell实验研究沉默SPAG5对细胞迁移和侵袭的影响。最后，WB检测细胞内磷酸肌醇3激酶（PI3K）和AKT的磷酸化水平。结果表明SPAG5在CRC中高表达并得到WB验证。 SPAG5 的沉默抑制了细胞活力和增殖并增加了细胞凋亡率。此外，SPAG5的低表达抑制了细胞侵袭和迁移能力。最后，WB结果发现SPAG5沉默后PI3K和AKT的磷酸化水平降低。综上所述，结果表明SPAG5可以通过靶向PI3K/AKT信号通路促进CRC细胞的增殖和侵袭。

Colorectal cancer (CRC) is a cancer that occurs in the rectum or colon with a high incidence. Sperm-associated antigen 5 (SPAG5), a gene that regulates cell division, has been observed highly expressed in a variety of cancers, but its role in CRC is unclear. This study aimed to investigate the regulatory role of SPAG5 in CRC. The expression of SPAG5 in multiple cancers and normal tissues was predicted by The Cancer Genome Atlas and Tumor Immune Estimation Resource, and the expression of SPAG5 in human normal intestinal epithelial cells NCM460 and human CRC cell lines Caco2, HT29, SW480, and LOVO was verified by western blotting (WB). The effects of silencing SPAG5 on cell viability, proliferation, and apoptosis were then investigated by cell counting kit-8, WB, and flow cytometry. The effects of silencing SPAG5 on cell migration and invasion were investigated by scratch assay and transwell assay. Finally, the phosphorylation levels of phosphoinositide 3-kinase (PI3K) and AKT in cells were detected by WB. The results showed that SPAG5 was highly expressed in CRC and was verified by WB. Silencing of SPAG5 inhibited cell viability and proliferation and increased the cell apoptosis rate. Furthermore, both cell invasion and migration abilities were suppressed by the low expression of SPAG5. Finally, WB results found that the phosphorylation levels of PI3K and AKT were reduced after SPAG5 silencing. In summary, the results showed that SPAG5 can promote the proliferation and invasion of CRC cells by targeting the PI3K/AKT signaling pathway.