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L1CAM Promotes Human Endometrial Cancer Via NF-κB Activation.

Hiroyuki Kurosu1,2, Hiroshi Asano2, Alaa-Eldin Salah-Eldin3

  • 1Department of Pathology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.

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L1 cell adhesion molecule (L1CAM) promotes endometrial cancer growth and chemoresistance by activating the NF-κB pathway. Targeting this L1CAM-NF-κB signaling offers a potential therapeutic strategy for improving patient outcomes.

Keywords:
L1CAMNF-κBcell cycledrug resistanceendometrial cancer

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Area of Science:

  • Gynecological Oncology
  • Molecular Oncology
  • Cancer Biology

Background:

  • Endometrial cancer incidence and mortality are rising globally.
  • L1 cell adhesion molecule (L1CAM) is a poor prognostic factor in endometrial cancer.
  • The precise molecular mechanisms of L1CAM in endometrial cancer progression are not fully understood.

Purpose of the Study:

  • To elucidate the biological role and molecular mechanisms of L1CAM in human endometrial cancer.
  • To investigate the association between L1CAM and the NF-κB signaling pathway.
  • To evaluate potential therapeutic strategies targeting the L1CAM pathway.

Main Methods:

  • Functional assays (proliferation, cell cycle, apoptosis) were conducted after L1CAM manipulation (knockdown/overexpression) in endometrial cancer cell lines.
  • NF-κB signaling pathway activation was assessed via Western blotting and immunohistochemistry.
  • Combination therapy effects were evaluated using cisplatin and an IKK inhibitor.

Main Results:

  • L1CAM overexpression enhanced endometrial cancer cell proliferation by promoting G0/G1 phase transition.
  • L1CAM knockdown inhibited NF-κB signaling, evidenced by reduced p65 phosphorylation and downstream target expression (e.g., TNF).
  • Restoration of proliferation upon IKKβ overexpression confirmed NF-κB as a key downstream mediator of L1CAM.
  • L1CAM expression positively correlated with nuclear NF-κB (p65) in patient samples.
  • Combined cisplatin and IKK inhibitor treatment showed enhanced anti-proliferative effects.

Conclusions:

  • L1CAM drives proliferation and chemoresistance in endometrial cancer via NF-κB pathway activation.
  • The L1CAM-NF-κB axis represents a critical pathway in endometrial cancer progression.
  • Targeting the L1CAM-NF-κB pathway presents a promising therapeutic avenue for L1CAM-positive endometrial cancer.