Background: STAM-binding protein-like 1 (STAMBPL1) functions as a deubiquitinase to cleave Lys63 ubiquitin linkage, and is associated with cancer dissemination and progression. The role of STAMBPL1 in colorectal cancer (CRC) remains unclear. Methods: STAMBPL1 expression was determined by western blot and qRT-PCR. Cell proliferation was detected by colony formation and MTT assays, and apoptosis was assessed by flow cytometry. The metastasis was evaluated by transwell and wound healing assays. An animal xenograft experiment was used to investigate the effect of STAMBPL1 on tumor growth. Results: The expression of STAMBPL1 was elevated in CRC cells. Knockdown of STAMBPL1 reduced cell viability of CRC and suppressed the proliferation, invasion, and migration. Apoptosis of CRC was induced by silence of STAMBPL1. Tumor growth of CRC was also suppressed by the silence of STAMBPL1. Knockdown of STAMBPL1 increased IκB and decreased phosphorylation of IκB to reduce p65 phosphorylation. Conclusion: Knockdown of STAMBPL1 inhibited cell growth and metastasis of CRC through inactivation of the NF-κB pathway.

中文翻译：

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STAM 结合蛋白样 1 通过 NF-κB 通路促进结直肠癌的生长和迁移


背景：STAM 结合蛋白样 1 (STAMBPL1) 作为去泛素酶来裂解 Lys63 泛素连接，并与癌症扩散和进展相关。 STAMBPL1 在结直肠癌 (CRC) 中的作用仍不清楚。方法：通过蛋白质印迹和 qRT-PCR 测定 STAMBPL1 表达。通过集落形成和MTT测定检测细胞增殖，并通过流式细胞术评估细胞凋亡。通过transwell和伤口愈合测定来评估转移。采用动物异种移植实验来研究 STAMBPL1 对肿瘤生长的影响。结果：CRC细胞中STAMBPL1的表达升高。 STAMBPL1 的敲低降低了 CRC 细胞的活力并抑制了增殖、侵袭和迁移。 STAMBPL1 沉默可诱导 CRC 凋亡。 STAMBPL1 的沉默也抑制了 CRC 的肿瘤生长。 STAMBPL1 的敲低会增加 IκB 并降低 IκB 的磷酸化，从而减少 p65 磷酸化。结论：STAMBPL1 的敲低通过 NF-κB 通路的失活抑制了 CRC 的细胞生长和转移。