IFITM10 Enhance Tumor Angiogenesis and Promotes Cancer Progression through STAT3 Activation

  • Front Biosci (Landmark Ed). 2024 Aug 16;29(8):283. doi: 10.31083/j.fbl2908283.
Youjian Li  1 Mengjie Wang  2 Xun Li  3 Jiehong Jia  1 Fei Pan  1 Wen Li  1 Zhongzhu Chen  1 Dianyong Tang  1 Kepeng Ou  1
Affiliations
  • 1. College of Pharmacy, National & Local Joint Engineering Research Center of Targeted and Innovative Therapeutics, IATTI, Chongqing University of Arts and Sciences, 402160 Chongqing, China.
  • 2. Tongji Medical College, Huazhong University of Science and Technology, 430074 Wuhan, Hubei, China.
  • 3. Institute for Viral Hepatitis, Chongqing Medical University, 400016 Chongqing, China.
Abstract

Background: 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.

Methods: The Cancer Genome Atlas database was analyzed for acquiring interferon-γ inducible protein 10 (IFITM10) 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.

Results: 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.

Conclusion: 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.

Keywords
IFITM10; STAT3 activation; angiogenesis; colorectal cancer.