ODF3B Promotes the Progression of Clear Cell Renal Cell Carcinoma via the JAK/STAT Signaling Pathway

Yongyang Yun1,2,3,4, Xing Ji1,2,3,4, Tianyu Wu1,2,3,4

  • 1Department of Urology, Peking University First Hospital, Beijing, China.

Insights

Outer dense fiber of sperm tails 3B (ODF3B) drives clear cell renal cell carcinoma (ccRCC) by activating Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling. High ODF3B expression indicates poor prognosis and aggressive ccRCC features, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Clear cell renal cell carcinoma (ccRCC) is a prevalent kidney cancer with poor prognosis due to metastasis and treatment resistance.
  • The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is a key driver in ccRCC, but its upstream regulators are not fully understood.
  • Outer dense fiber of sperm tails 3B (ODF3B) is dysregulated in ccRCC, yet its functional role remains unclear.

Purpose of the Study:

  • To investigate the role of Outer dense fiber of sperm tails 3B (ODF3B) in clear cell renal cell carcinoma (ccRCC).
  • To determine the prognostic significance of ODF3B in ccRCC.
  • To elucidate the mechanism by which ODF3B influences ccRCC progression, particularly its connection to the JAK/STAT pathway.

Main Methods:

  • Analysis of ODF3B expression in The Cancer Genome Atlas (TCGA) and ccRCC cell lines.
  • Functional assays (proliferation, migration, invasion, apoptosis) following ODF3B knockdown.
  • Bioinformatic analyses for pathway enrichment and Western blotting to explore molecular mechanisms.
  • Rescue experiments using a STAT3 agonist (Colivelin TFA).

Main Results:

  • ODF3B is significantly upregulated in ccRCC tissues and cells, correlating with advanced stage, metastasis, and poorer survival.
  • ODF3B knockdown inhibited ccRCC cell proliferation, migration, and invasion, while promoting apoptosis.
  • ODF3B dysregulation was linked to the activation of JAK/STAT signaling, with ODF3B knockdown decreasing JAK/STAT phosphorylation.

Conclusions:

  • ODF3B functions as an oncogenic driver in ccRCC by activating the JAK/STAT signaling pathway.
  • Elevated ODF3B expression is a predictor of aggressive ccRCC and poor patient outcomes.
  • ODF3B represents a potential therapeutic target for ccRCC treatment.

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