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Integrated Multi-Omics and Spatial Transcriptomics Identify FBLL1 as a Malignant Transformation Driver in

Junye Xie1,2,3,4,5,6, Shujun Guo1,2,3,4,5,6, Yujie Xiao1,2,3,4,5,6

  • 1Institute of Biomedicine & Department of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.

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|February 12, 2026
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Summary

FBLL1 is a newly found gene that drives liver cancer (hepatocellular carcinoma) progression by activating key growth pathways. Targeting FBLL1 may offer a new strategy for treating liver cancer.

Keywords:
EGFR signalingFBLL1c-Mychepatocellular carcinomamalignant transformationspatial transcriptomics

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Hepatocellular carcinoma (HCC) exhibits significant intratumoral heterogeneity and leads to poor patient outcomes.
  • Dysregulated ribosome biogenesis is a known hallmark of cancer, but its specific role in HCC pathogenesis is unclear.
  • Identifying novel molecular drivers is crucial for understanding and treating HCC.

Purpose of the Study:

  • To identify and characterize novel prognostic candidate genes in hepatocellular carcinoma.
  • To elucidate the molecular mechanisms by which these genes contribute to HCC progression.
  • To evaluate potential therapeutic targets for liver cancer.

Main Methods:

  • Integration of multi-omics data from TCGA and ICGC cohorts to identify candidate genes.
  • Analysis of gene distribution using single-cell RNA sequencing and spatial transcriptomics.
  • In vitro and in vivo functional validation through gene knockdown and overexpression experiments.
  • Elucidation of molecular mechanisms via transcriptomic analysis and Western blotting.

Main Results:

  • FBLL1 was identified as a key prognostic gene, significantly upregulated in HCC and associated with poor survival.
  • FBLL1 expression was enriched in malignant hepatocytes within tumors.
  • FBLL1 knockdown inhibited HCC cell proliferation, while its overexpression promoted tumorigenesis in vivo.
  • FBLL1 overexpression correlated with increased c-Myc and EGFR ligands, impacting the EGFR-MAPK pathway.

Conclusions:

  • FBLL1 is a novel regulator implicated in the malignant transition of HCC.
  • FBLL1 promotes HCC by facilitating ligand-dependent EGFR-MAPK pathway activation alongside c-Myc upregulation.
  • FBLL1 represents a potential therapeutic target for disrupting oncogenic signaling in liver cancer.