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Peer-reviewedCC BY 4.0PLOS One

BCAM-AKT2 fusion protein promotes unfolded protein response driven oncogenic signaling in SKOV3 epithelial ovarian cancer cell line

  • Hala Khazem1
  • Ravid Solomon Zemler2
  • Liron Vardi David3
  • Dvir Reder4
  • Shilhav Meisel Sharon
  • Shay Hantisteanu
  • Haim Werner
  • Ilan Bruchim
4 affiliations
  1. 1Gynecologic Oncology Laboratory, Division of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Hadera, Israel
  2. 2The Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel
  3. 3Division of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Hadera, Israel
  4. 4Department of Human Molecular Genetics and Biochemistry, Gray Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel
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Abstract

In view of the rapidly increasing evidence that gene fusion mutations are frequent drivers of cancer, a deeper understanding of the molecular and functional hallmarks of specific gene fusions in epithelial ovarian cancer (EOC) is essential. In this work we sought to identify the molecular signature of the BCAM-AKT2 fusion protein in ovarian cancer cell lines and to assess the biological impact of the novel fusion in these cells. Our in-vitro results show that the BCAM-AKT2 fusion protein is engaged in proliferative action within EOC cell lines. Furthermore, RNA-seq analysis shows that the effect of BCAM-AKT2 in SKOV3 cells is associated with activated unfolded protein response (UPR) and with the inhibition of interferon alpha and beta signaling pathways, pyropstosis and viral response in EOC cell lines. Overall, our results indicate that in SKOV3 cells, BCAM-AKT2 modulates the UPR signaling pathway, which is known to interact with oncogene and tumor suppressor networks during cancer development. These findings offer fresh insights suggesting that BCAM-AKT2 could serve as a promising target for therapeutic interventions in ovarian cancer.

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Cite

BibTeXRIS
BibTeX
@article{khazem2026bcamakt2,
  title = {{BCAM-AKT2 fusion protein promotes unfolded protein response driven oncogenic signaling in SKOV3 epithelial ovarian cancer cell line}},
  author = {Hala Khazem and Ravid Solomon Zemler and Liron Vardi David and Dvir Reder and Shilhav Meisel Sharon and Shay Hantisteanu and Haim Werner and Ilan Bruchim},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0357882},
  url = {https://doi.org/10.1371/journal.pone.0357882},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - BCAM-AKT2 fusion protein promotes unfolded protein response driven oncogenic signaling in SKOV3 epithelial ovarian cancer cell line
AU  - Hala Khazem
AU  - Ravid Solomon Zemler
AU  - Liron Vardi David
AU  - Dvir Reder
AU  - Shilhav Meisel Sharon
AU  - Shay Hantisteanu
AU  - Haim Werner
AU  - Ilan Bruchim
PY  - 2026
DA  - 2026/09/25
JO  - PLOS One
DO  - 10.1371/journal.pone.0357882
UR  - https://doi.org/10.1371/journal.pone.0357882
AB  - In view of the rapidly increasing evidence that gene fusion mutations are frequent drivers of cancer, a deeper understanding of the molecular and functional hallmarks of specific gene fusions in epithelial ovarian cancer (EOC) is essential. In this work we sought to identify the molecular signature of the BCAM-AKT2 fusion protein in ovarian cancer cell lines and to assess the biological impact of the novel fusion in these cells. Our in-vitro results show that the BCAM-AKT2 fusion protein is engaged in proliferative action within EOC cell lines. Furthermore, RNA-seq analysis shows that the effect of BCAM-AKT2 in SKOV3 cells is associated with activated unfolded protein response (UPR) and with the inhibition of interferon alpha and beta signaling pathways, pyropstosis and viral response in EOC cell lines. Overall, our results indicate that in SKOV3 cells, BCAM-AKT2 modulates the UPR signaling pathway, which is known to interact with oncogene and tumor suppressor networks during cancer development. These findings offer fresh insights suggesting that BCAM-AKT2 could serve as a promising target for therapeutic interventions in ovarian cancer.
SN  - 1932-6203
ER  -