Full-Length Transcriptome Profiles Reveal the Molecular Function of Oncogene HNRNPA2B1 in Triple-Negative Breast

Lina Yi1, Yongtao Li1, Jianghua Ou1

  • 1Department of Breast Surgery, Xinjiang Medical University Affiliated Tumor Hospital, Urumqi, Xinjiang, China.

Cancer Medicine
|May 10, 2026
PubMed

Insights

Heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1) drives triple-negative breast cancer (TNBC) growth and metastasis. Inhibiting HNRNPA2B1 in TNBC cells suppressed proliferation and metastasis, offering potential therapeutic strategies.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis.
  • Aberrant expression of Heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1), an RNA-binding protein, is linked to poor outcomes in various cancers.
  • The role and mechanisms of HNRNPA2B1 in TNBC remain largely uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of HNRNPA2B1 in TNBC.
  • To elucidate the molecular mechanisms by which HNRNPA2B1 influences TNBC progression.
  • To assess the therapeutic potential of targeting HNRNPA2B1 in TNBC.

Main Methods:

  • Examined HNRNPA2B1 expression in normal and TNBC cell lines.
  • Performed in vitro and in vivo knockdown experiments of HNRNPA2B1 in TNBC cells.
  • Analyzed changes in cell proliferation, metastasis, apoptosis, gene expression, and alternative splicing using various techniques, including Nanopore long-read sequencing.

Main Results:

  • HNRNPA2B1 is significantly overexpressed in TNBC tissues and cell lines.
  • Knockdown of HNRNPA2B1 inhibited TNBC cell proliferation and metastasis, while promoting apoptosis.
  • HNRNPA2B1 knockdown altered gene expression and alternative splicing, impacting cell migration, proliferation, and apoptosis pathways.
  • Nanopore sequencing revealed HNRNPA2B1 regulates gene expression via alternative polyadenylation modulation.

Conclusions:

  • HNRNPA2B1 is a critical oncogene in TNBC progression.
  • Targeting HNRNPA2B1 demonstrates potential for novel therapeutic strategies in TNBC.
  • Understanding HNRNPA2B1's role in alternative polyadenylation provides new mechanistic insights into TNBC development.

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