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KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1

  • Authors:
    • Jing Yang
    • Rongxia He
    • Xiaoling Zhang
    • Xing Wang
    • Min Liu
    • Xiaolong Liu
    • Yulan Li
  • View Affiliations / Copyright

    Affiliations: The First School of Clinical Medical, Lanzhou University, Lanzhou, Gansu 730000, P.R. China, Department of Obstetrics, Lanzhou University Second Hospital, Lanzhou, Gansu 730000, P.R. China, Department of Pathology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 67
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    Published online on: April 16, 2025
       https://doi.org/10.3892/or.2025.8900
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Abstract

Ovarian cancer (OC) is a prevalent malignancy; however, the role of kinesin light chain 3 (KLC3) in OC remains unclear. The present study conducted a comprehensive investigation of KLC3 using bioinformatics analysis, as well as in vitro and in vivo experiments. The findings revealed that KLC3 expression was significantly upregulated in the OC group compared with that in the normal group, and high KLC3 expression in patients with OC was associated with a poorer overall survival. Functional studies demonstrated that targeting KLC3 effectively suppressed the proliferation, migration, epithelial‑mesenchymal transition and DNA damage resistance of OC cells in vitro, while also inhibiting tumor growth in vivo, underscoring the pivotal role of KLC3 in tumor progression and metastasis. Additionally, RNA‑sequencing analysis identified collagen type III α1 (COL3A1) as a potential downstream gene cooperating with KLC3 to promote the occurrence and development of OC through the PI3K/AKT signaling pathway. Rescue experiments revealed that the KLC3 knockdown‑induced suppression of the malignant phenotype could be partially reversed by overexpression of COL3A1. In summary, the present findings demonstrated that KLC3 acts as an oncogene by influencing COL3A1 expression to promote the proliferation and migration of OC cells in vivo and in vitro.
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Copy and paste a formatted citation
Spandidos Publications style
Yang J, He R, Zhang X, Wang X, Liu M, Liu X and Li Y: KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1. Oncol Rep 53: 67, 2025.
APA
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., & Li, Y. (2025). KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1. Oncology Reports, 53, 67. https://doi.org/10.3892/or.2025.8900
MLA
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., Li, Y."KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1". Oncology Reports 53.6 (2025): 67.
Chicago
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., Li, Y."KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1". Oncology Reports 53, no. 6 (2025): 67. https://doi.org/10.3892/or.2025.8900
Copy and paste a formatted citation
x
Spandidos Publications style
Yang J, He R, Zhang X, Wang X, Liu M, Liu X and Li Y: KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1. Oncol Rep 53: 67, 2025.
APA
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., & Li, Y. (2025). KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1. Oncology Reports, 53, 67. https://doi.org/10.3892/or.2025.8900
MLA
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., Li, Y."KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1". Oncology Reports 53.6 (2025): 67.
Chicago
Yang, J., He, R., Zhang, X., Wang, X., Liu, M., Liu, X., Li, Y."KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1". Oncology Reports 53, no. 6 (2025): 67. https://doi.org/10.3892/or.2025.8900
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