RNAseq-based meta-analyses revealed tumor suppressor-inducer fusion events in liver, oral, and ovarian cancer in the Indian population: a cancer cell surviving mechanism.

Cancer cell characteristics are determined by gene expression, influenced by genomic, epigenetic, and transcriptional modifications. Genomic rearrangements and transcriptional splicing can result in the formation of fusion genes. BCR-ABL1 is an established fusion gene employed as a biomarker in leukemia. A single gene can amalgamate with several other genes and may impact cellular fate. Ethnicity-specific variants of fusion genes have been identified, such as the TMPRSS2-ERG variation observed in prostate malignancies among African-American, Caucasian, and Japanese populations in research studies. Next-generation sequencing has provided a new method for predicting genomic and transcriptomic changes. We aim to identify fusion genes in the Indian population using cancer samples to enhance diagnostic outcomes. This study performed a meta-analysis of tumor-specific RNA sequencing data for liver, tongue, and ovarian cancers, which are available online. It identified known fusion genes, including TRO-MAGED2, KRT14-S100A9, RNASE10-CD38, ACTN4-ACTN1, RGPD1-RANBP2, CTSC-RAB38, C15orf57-CBX3, AMBRA1-CKAP5, ATP2B3-ATP2B4, CNKSR3-IPCEF1, E2F4-RPL14, and MZT2A-MZT2B, along with 101 novel fusion genes. Novel fusion genes GABRP_SCGB3A2 and WWOX_FUT1 were identified in all three tumor tissues. GABRP acts as a tumor inducer, whereas SCGB3A2 functions as a tumor suppressor. WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

• Publication year

  2026

• Venue

  Nucleosides, Nucleotides & Nucleic Acids

• Publication date

  2026-02-09

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1080/15257770.2026.2624447PMID 41661231
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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