The Desmoid Tumor Research Foundation

March 2025

Chlorhexidine dihydrochloride shows anti-tumor effects in desmoid tumors and colorectal cancer

Author Information

Hyeran Shin # 1 2, Yonghyo Kim # 1, Yehyeong Lee 1 3, Jisoo Kim 1 3, Yeong Chan Ryu 4, Dong-Woo Kang 5, Tae Il Kim 6, Yong-Hee Cho 7 2

1Drug Discovery Platform Research Center, Therapeutics and Biotechnology Division, Korea Research Institute of Chemical Technology (KRICT), Daejeon, Republic of Korea.2Department of Biotechnology, Yonsei University, Seoul, Republic of Korea.3Department of Medicinal Chemistry and Pharmacology, University of Science and Technology (UST), Daejeon, Republic of Korea.4Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea.5Medpacto Inc., Seoul, Republic of Korea.6Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.7Drug Discovery Platform Research Center, Therapeutics and Biotechnology Division, Korea Research Institute of Chemical Technology (KRICT), Daejeon, Republic of Korea; y-hcho@krict.re.kr.#Contributed equally.

Publication

Anticancer Res.

Summary

BACKGROUND/AIM: Desmoid tumors (DTs), or aggressive fibromatosis, are rare neoplasms arising from connective tissue, frequently exhibiting local invasiveness. The limited treatment options and high recurrence rates of DTs highlight the need for novel therapeutic strategies. This study investigated the efficacy of chlorhexidine dihydrochloride (CD) in inhibiting the growth of DTs and colorectal cancer (CRC). MATERIALS AND METHODS: A mouse model with Apc mutations, specifically Apc1638N/+, was generated to study DTs. DT cells (Apc1638N+) (DTA) were collected from the mice for in vitro experiments. DTA were treated with CD, along with a CRC cell line (HCT-116), and tumor organoids derived from Apc1638N/+ mice. The effects of CD were assessed through cell viability assay (WST assay), colony formation assay, and cell migration assay. We tested the induction of cell apoptosis through caspase 3/7 activity assays and immunoblot analysis of cleaved-caspase 3 and cleaved-PARP1. Additionally, CD was tested for its anti-tumor efficacy using an in vivo CRC xenograft model with the HCT-116 cell line. RESULTS: CD significantly inhibited the viability, migration, and colony formation of DTA and CRC cells. It remarkably decreased the tumor growth in organoids derived from intestinal tumor cells in the Apc1638N/+ mouse model. Furthermore, CD showed anti-tumor effects in an in vivo CRC xenograft model using the HCT-116 cell line. CONCLUSION: CD represents a promising therapeutic strategy for treating both DTs and CRC.

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