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<p>The present study identifies a novel intergenic mRNA trans-splicing event that generates a previously uncharacterized chimeric transcript comprising family with sequence similarity 168&#xa0;member B (FAM168B), and ankyrin repeat domain 42 (ANKRD42) in prostate cancer. DNA and RNA sequencing (RNA-seq) analyses revealed the formation of a novel chimeric mRNA, FAM168B::ANKRD42, arising from intergenic mRNA trans-splicing. This finding is supported by chimeric split reads at the RNA level and their absence at the DNA level, consistent with a trans-splicing mechanism rather than a genomic rearrangement. Open reading frame (ORF) prediction suggests that FAM168B::ANKRD42 transcript encodes a novel fusion peptide. Integrative bio-computational analyses, including kinase enrichment and transcription factor profiling, identified key regulatory molecules such as AKT1 serine/threonine kinase 1 (AKT1), androgen receptor (AR), forkhead box A1 (FOXA1), and E2F transcription factor 1 (E2F1), indicating potential involvement in transcriptional regulation and cell cycle control. Sequence-based predictions further suggest that the chimeric FAM168B::ANKRD42 peptide may harbor AKT1 phosphorylation sites, thereby potentially modulating the AR/FOXA1 signaling axis, leading to activation of E2F1 and downstream S-phase gene expression. In conclusion, this study provides novel insights into the functional role of FAM168B as a potential facilitator of cell cycle progression and highlights the chimeric FAM168B::ANKRD42 peptide as a putative driver of prostate cancer progression.</p>

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Intergenic trans-splicing–driven formation of a chimeric FAM168B::ANKRD42 transcript in prostate cancer

  • 期刊论文

  • 发表日期：

    2026年6月25日

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  • Sidharth Dash Sharma,
  • Sreemoyee Sensharma,
  • Arne Kutzner,
  • Gopal Pramanik,
  • Klaus Heese,
  • Subrata Pramanik

摘要

The present study identifies a novel intergenic mRNA trans-splicing event that generates a previously uncharacterized chimeric transcript comprising family with sequence similarity 168 member B (FAM168B), and ankyrin repeat domain 42 (ANKRD42) in prostate cancer. DNA and RNA sequencing (RNA-seq) analyses revealed the formation of a novel chimeric mRNA, FAM168B::ANKRD42, arising from intergenic mRNA trans-splicing. This finding is supported by chimeric split reads at the RNA level and their absence at the DNA level, consistent with a trans-splicing mechanism rather than a genomic rearrangement. Open reading frame (ORF) prediction suggests that FAM168B::ANKRD42 transcript encodes a novel fusion peptide. Integrative bio-computational analyses, including kinase enrichment and transcription factor profiling, identified key regulatory molecules such as AKT1 serine/threonine kinase 1 (AKT1), androgen receptor (AR), forkhead box A1 (FOXA1), and E2F transcription factor 1 (E2F1), indicating potential involvement in transcriptional regulation and cell cycle control. Sequence-based predictions further suggest that the chimeric FAM168B::ANKRD42 peptide may harbor AKT1 phosphorylation sites, thereby potentially modulating the AR/FOXA1 signaling axis, leading to activation of E2F1 and downstream S-phase gene expression. In conclusion, this study provides novel insights into the functional role of FAM168B as a potential facilitator of cell cycle progression and highlights the chimeric FAM168B::ANKRD42 peptide as a putative driver of prostate cancer progression.