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STK32C as a Therapeutic Target in Colorectal Cancer via HSP90-PI3K/AKT/mTOR Signaling

Chi-Hoon Ahn1, Ji Eon Park1, Deok Yong Sim1

  • 1Cancer Molecular Targeted Herbal Research Laboratory, College of Korean Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 02447, South Korea.

International Journal of Biological Sciences
|November 10, 2025
PubMed

Insights

Serine/threonine kinase 32C (STK32C) drives colorectal cancer (CRC) by interacting with HSP90 and activating PI3K/AKT/mTOR signaling. Targeting STK32C may enhance chemotherapy efficacy, offering a new therapeutic strategy for CRC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Serine/threonine kinase 32C (STK32C) is implicated in other cancers but its role in colorectal cancer (CRC) is unknown.
  • Understanding STK32C's function in CRC is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the oncogenic mechanism of STK32C in colorectal cancer (CRC).
  • To explore the interplay between STK32C, HSP90, and the PI3K/AKT/mTOR signaling pathway in CRC.
  • To evaluate STK32C as a potential therapeutic target in CRC, alone or in combination with 5-fluorouracil (5-FU).

Main Methods:

  • Upregulation of STK32C in CRC cell lines was assessed via expression analysis.
  • Cellular functions (proliferation, migration, invasion, apoptosis) were evaluated upon STK32C depletion.
  • Protein interactions were confirmed using immunoprecipitation, immunofluorescence, and GST pulldown assays.
  • Signaling pathway modulation was analyzed using specific inhibitors and Western blotting.
  • Synergistic effects with 5-FU were determined using CompuSyn and SynergyFinder.
  • Tumorigenicity was assessed in a mouse xenograft model.

Main Results:

  • STK32C was significantly upregulated in CRC cell lines and associated with poor prognosis.
  • STK32C depletion inhibited CRC cell proliferation, migration, and invasion, while promoting apoptosis.
  • STK32C directly binds to HSP90 and acts upstream of AKT in the PI3K/AKT/mTOR pathway.
  • STK32C depletion synergistically enhanced the efficacy of 5-FU chemotherapy.
  • In vivo studies confirmed that STK32C depletion suppressed tumor growth and modulated related signaling pathways.

Conclusions:

  • STK32C is a novel oncogenic driver in colorectal cancer.
  • STK32C modulates HSP90 and PI3K/AKT/mTOR signaling, contributing to CRC progression.
  • Targeting STK32C presents a promising therapeutic strategy for colorectal cancer, potentially enhancing chemotherapy response.
Keywords:
ApoptosisColorectal cancerHSP90PI3K/AKT/mTOR.STK32C

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