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FAT10: Function and Relationship with Cancer.

Senfeng Xiang1, Xuejing Shao1, Ji Cao1

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The ubiquitin-like modifier FAT10 (also known as FAT10) is upregulated in many cancers, influencing cell proliferation, invasion, and metastasis. This review summarizes FAT10

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Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Posttranslational protein modifications play a crucial role in cancer development.
  • The ubiquitin-like modifier FAT10 (also known as FAT10) is increasingly recognized for its direct involvement in oncogenesis.
  • FAT10 is significantly upregulated across diverse cancer types, including glioma, hepatocellular carcinoma, breast, and gastrointestinal cancers.

Purpose of the Study:

  • To review the current understanding of FAT10's biological functions in cancer.
  • To discuss the mechanisms by which FAT10 influences cancer progression.
  • To explore potential therapeutic strategies targeting the FAT10 pathway.

Main Methods:

  • Literature review of studies on FAT10 and cancer.
  • Analysis of FAT10's role in protein modification.
  • Examination of FAT10's impact on cancer cell behavior.

Main Results:

  • FAT10ylation and FAT10 interactions alter protein function, affecting proteasomal degradation, subcellular localization, and stability.
  • These modifications significantly impact cancer cell proliferation, invasion, metastasis, and tumorigenesis.
  • FAT10 upregulation is a common feature in various human malignancies.

Conclusions:

  • FAT10 is a key player in cancer development and progression.
  • Targeting the FAT10 pathway presents a promising avenue for novel cancer therapies.
  • Further research into FAT10's mechanisms and therapeutic potential is warranted.