College of Pharmacy, National & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, IATTI, Chongqing University of Arts and Sciences, 402160 Chongqing, China.
Tongji Medical College, Huazhong University of Science and Technology, 430074 Wuhan, Hubei, China.
Front Biosci (Landmark Ed). 2024 Aug 16;29(8):283. doi: 10.31083/j.fbl2908283.
Humankind have been struggling with colorectal cancer (CRC) for long period with its rapid progression and invasive metastasis. By hyperactivating IL-6/STAT3 signaling, CRC facilitates the capacity of angiogenesis to plunder massive nutrients and develops gradually under harsh condition.
The Cancer Genome Atlas database was analyzed for acquiring interferon-γ inducible protein 10 () expression levels and their correlation with clinical outcomes. The cell angiogenic ability were assessed by Cell Counting Kit-8 (CCK-8) and tube formation assay. Immunofluorescence, Western blot, and enzyme-linked immunosorbent assay (ELISA) assay were using to assess potential mechanism.
In our study, we find that IFITM10 is upregulated in CRC and is positively related with tumor angiogenesis. We also find that IFITM inhibition decreased STAT3 phosphorylation level and IFITM10-mediated angiogenesis depends on STAT3 activation. Furthermore, our data suggests that IFITM10 may be a key prognostic biomarker in colorectal cancer.
Together, our study suggests that IFITM10 enhance angiogenesis through STAT3 activation during CRC progression, which highlighting its potency as a therapeutic target for colorectal cancer.
结直肠癌（CRC）进展迅速且具有侵袭性转移，人类与之抗争已久。CRC 通过过度激活 IL-6/STAT3 信号通路，促进血管生成能力掠夺大量营养物质，并在恶劣条件下逐渐发展。
分析癌症基因组图谱数据库获取干扰素诱导蛋白 10（IFITM10）的表达水平及其与临床结局的相关性。通过细胞计数试剂盒-8（CCK-8）和管形成试验评估细胞的血管生成能力。免疫荧光、Western blot 和酶联免疫吸附试验（ELISA）检测用于评估潜在机制。
在本研究中，我们发现 IFITM10 在 CRC 中上调，并与肿瘤血管生成呈正相关。我们还发现，IFITM 抑制降低了 STAT3 磷酸化水平，IFITM10 介导的血管生成依赖于 STAT3 的激活。此外，我们的数据表明，IFITM10 可能是结直肠癌的一个关键预后生物标志物。
综上所述，我们的研究表明，IFITM10 通过 CRC 进展过程中的 STAT3 激活增强血管生成，凸显其作为结直肠癌治疗靶点的潜力。
