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Updated: May 22, 2025

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KIF3C inhibits the progression and proliferation of colorectal cancer

Maladho Tanta Diallo1,2,3,4, Bangquan Chen1,2,4, Qing Yao1,2,4

  • 1Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, China.

BMC Gastroenterology
|March 13, 2025
PubMed
Abstract

Insights

Kinesin heavy chain 3C (KIF3C) is upregulated in colorectal cancer (CRC), promoting tumor growth and progression. Inhibiting KIF3C may offer a new therapeutic strategy for CRC treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Kinesin superfamily motor protein KIF3C is upregulated in multiple cancers.
  • KIF3C influences cancer cell proliferation, migration, and invasion.
  • KIF3C's role in colorectal cancer (CRC) requires further investigation.

Purpose of the Study:

  • To investigate the expression and function of KIF3C in colorectal cancer.
  • To determine the correlation between KIF3C expression and CRC prognosis.
  • To explore KIF3C's impact on CRC cell behavior and signaling pathways.

Main Methods:

  • Immunohistochemistry, Western blot, and RT-qPCR were used to assess KIF3C expression in CRC tissues and cells.
  • KIF3C was manipulated (knockdown and overexpression) using lentiviral vectors in CRC cell lines (SW-480, HCT-116, SW-620).
  • In vitro assays (transwell, scratch wound healing, colony formation, CCK-8) and signaling pathway analyses were performed.

Main Results:

  • KIF3C is highly expressed in CRC cells and tissues, correlating with poor prognosis.
  • KIF3C knockdown significantly inhibited proliferation and migration in CRC cells.
  • KIF3C upregulation promoted CRC progression via the PI3K/AKT, Bax, and Bcl-2 pathways.

Conclusions:

  • KIF3C knockdown inhibits colorectal cancer cell proliferation and migration.
  • KIF3C plays a crucial role in CRC progression.
  • KIF3C represents a potential therapeutic target for colorectal cancer treatment.
Keywords:
Cell cycleColorectal cancerKIF3CProliferationSignaling pathway

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