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Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
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.
Abstract:
BACKGROUND Clear cell renal cell carcinoma (ccRCC) is the most common renal malignancy, often associated with poor prognosis due to metastasis and treatment resistance. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is a major oncogenic driver in ccRCC, but its upstream regulators remain unclear. Outer dense fiber of sperm tails 3B (ODF3B), initially identified in sperm flagella, shows aberrant expression in a subset of human malignancies, and emerging transcriptomic data suggest notable dysregulation of ODF3B in ccRCC, although its functional role in this tumor type remains unknown. MATERIAL AND METHODS ODF3B expression was analyzed using data from The Cancer Genome Atlas (TCGA) and validated in ccRCC cell lines. Prognostic significance was evaluated through clinicopathological and survival analyses. Functional assays, including Cell Counting Kit 8, colony formation, wound healing, Transwell assay, and flow cytometry, were performed after ODF3B knockdown in 786-O and OSRC-2 cells. Pathway enrichment analyses and Western blotting were used to explore mechanisms, and rescue experiments were conducted with the STAT3 agonist Colivelin TFA. RESULTS ODF3B was markedly upregulated in ccRCC tissues and cells, with high expression correlating with advanced stage, metastasis, and poor survival. ODF3B silencing suppressed proliferation, migration, and invasion while enhancing apoptosis, accompanied by reduced BCL2 and increased cleaved caspase-3. Bioinformatics revealed strong enrichment of JAK/STAT signaling in tumors with high expression of ODF3B. Mechanistically, ODF3B knockdown decreased phosphorylation of JAK1/2/3 and STAT3, whereas STAT3 activation rescued proliferative and anti-apoptotic effects. CONCLUSIONS ODF3B acts as a novel oncogenic driver in ccRCC by activating JAK/STAT signaling. Its overexpression predicts aggressive features and poor prognosis, highlighting ODF3B as a potential therapeutic target.
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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