Zhu Wenjie, Wu Changlei, Liu Zitao, Zhao Shimin, Cheng Xiufeng, Huang Jun
Department of Gastrointestinal Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.
Jiangxi Province Key Laboratory of Molecular Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.
Cancer Cell Int. 2024 Jun 6;24(1):201. doi: 10.1186/s12935-024-03383-5.
Colorectal cancer (CRC) has the third highest incidence and second mortality rate of malignant tumors globally, highlighting the urgency to explore the mechanisms underlying CRC progression for refined treatment of this patient population.
R Studio was used for data sorting and analysis. Cell apoptosis and cell cycle detection were performed by flow cytometry. Quantitative real-time PCR (qRT-PCR) was used to explore mRNA expression levels. Western blotting was used to explore protein expression levels. CCK8, EdU, and colony formation assays were performed to explore the proliferation capacity of CRC cells. Transwell invasion and migration assays, along with the wound healing assay, were used to explore the invasive and migratory abilities of CRC cells. Subcutaneous Xenograft Assay was utilized to evaluate the tumorigenic capacity of CRC cells in vivo.
SULF1 was highly expressed in CRC samples and cell lines. The knockdown of SULF1 inhibited the proliferation, invasion, and migration of CRC and increased the rate of cell apoptosis. Meanwhile, we demonstrated that SULF1 could negatively regulate ARSH through the FAK/PI3K/AKT/mTOR pathway.
We demonstrated that SULF1 could promote CRC progression by regulating ARSH. The SULF1/ARSH/FAK/PI3K/AKT/mTOR signaling pathway represents a promising target for the treatment of this patient population. Colorectal cancer (CRC) has the third highest incidence and second mortality rate of malignant tumors globally. Sulfatase 1 (SULF1) belongs to the sulfatase family, The function of SULF1 in CRC remains elusive. Our study demonstrated that the knockdown of SULF1 could inhibit the proliferation, invasion, and migration of CRC. Meanwhile, our findings indicated that SULF1 could interact with Arylsulfatase Family Member H (ARSH) to regulate the proliferation, invasion, and migration of CRC via the FAK/PI3K/AKT/mTOR signaling pathway. Taken together, our findings suggest that SULF1 might be a new therapeutic target in CRC.
结直肠癌（CRC）的发病率在全球恶性肿瘤中位列第三，死亡率位列第二，这凸显了探索CRC进展机制以优化该患者群体治疗方案的紧迫性。
使用R Studio进行数据整理和分析。通过流式细胞术进行细胞凋亡和细胞周期检测。采用定量实时聚合酶链反应（qRT-PCR）来探究mRNA表达水平。利用蛋白质免疫印迹法来探究蛋白质表达水平。进行CCK8、EdU和集落形成实验以探究CRC细胞的增殖能力。采用Transwell侵袭和迁移实验以及伤口愈合实验来探究CRC细胞的侵袭和迁移能力。利用皮下异种移植实验评估CRC细胞在体内的致瘤能力。
SULF1在CRC样本和细胞系中高表达。敲低SULF1可抑制CRC的增殖、侵袭和迁移，并提高细胞凋亡率。同时，我们证明SULF1可通过FAK/PI3K/AKT/mTOR信号通路负向调节ARSH。
我们证明SULF1可通过调节ARSH促进CRC进展。SULF1/ARSH/FAK/PI3K/AKT/mTOR信号通路是该患者群体治疗的一个有前景的靶点。结直肠癌（CRC）的发病率在全球恶性肿瘤中位列第三，死亡率位列第二。硫酸酯酶1（SULF1）属于硫酸酯酶家族，SULF1在CRC中的功能仍不清楚。我们的研究表明，敲低SULF1可抑制CRC的增殖、侵袭和迁移。同时，我们的研究结果表明，SULF1可与芳基硫酸酯酶家族成员H（ARSH）相互作用，通过FAK/PI3K/AKT/mTOR信号通路调节CRC的增殖、侵袭和迁移。综上所述，我们的研究结果表明SULF1可能是CRC的一个新的治疗靶点。
