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Spindle function and Wnt pathway inhibition by PBX1 to suppress tumor progression via downregulating DCDC2 in

Weigang Dai1,2, Yinan Liu1,2,3, Tianhao Zhang1,2

  • 1Division of Gastrointestinal Surgery Center, the First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, Guangdong, P. R. China.

Oncogenesis
|February 4, 2023
PubMed

Insights

PBX1 acts as an antioncogene in colorectal cancer (CRC). Overexpressing PBX1 suppresses tumor growth and metastasis by inhibiting DCDC2 expression, disrupting spindle function, and modulating the Wnt pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • PBX1 is a transcription factor regulating lipid metabolism and cell proliferation.
  • Its role in various cancers is known, but its function in colorectal cancer (CRC) remains unstudied.
  • PBX1's dual role necessitates investigation in specific cancer contexts.

Purpose of the Study:

  • To elucidate the anti-tumor function of PBX1 in colorectal cancer (CRC).
  • To identify the molecular mechanisms underlying PBX1's action in CRC.
  • To determine PBX1's potential as a therapeutic target in CRC.

Main Methods:

  • Bioinformatics analysis to assess PBX1 expression in CRC.
  • In vitro and in vivo experiments to evaluate the effects of PBX1 overexpression.
  • Mechanistic studies involving gene expression analysis (DCDC2) and pathway investigation (Wnt).

Main Results:

  • PBX1 is significantly downregulated in CRC, suggesting antioncogenic activity.
  • PBX1 overexpression suppressed tumor growth and metastasis in CRC models.
  • PBX1 functions by suppressing DCDC2 expression, inhibiting spindle function, and impacting the Wnt pathway.

Conclusions:

  • PBX1 acts as a tumor suppressor in colorectal cancer.
  • The PBX1-DCDC2 axis is a critical regulator of CRC progression via spindle and Wnt pathway modulation.
  • Targeting PBX1 may offer a novel therapeutic strategy for colorectal cancer.

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