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JI-CJ001 Enhances Paclitaxel Sensitivity in Gastric Cancer Cell Lines through Inhibition of HER2/mTOR Signaling and

Min-Woo Kim1, Sang-Eun Lee1, So Eun Park2

  • 1Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Republic of Korea.

Anticancer Research
|March 27, 2026
PubMed
Abstract

Insights

JI-CJ001 enhances paclitaxel (PTX) effectiveness against gastric cancer by modulating HER2 signaling and autophagy. This combination therapy shows significant anti-tumor effects, offering a promising approach to overcome chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Chemoresistance is a major hurdle in cancer therapy, with HER2 signaling and autophagy pathways implicated in drug resistance.
  • Paclitaxel (PTX) is a standard chemotherapeutic agent, but its efficacy can be limited by resistance mechanisms.
  • The natural compound JI-CJ001 has demonstrated anticancer properties, but its combined effect with PTX in gastric cancer is not well understood.

Purpose of the Study:

  • To investigate if JI-CJ001 can enhance gastric cancer cell sensitivity to PTX.
  • To elucidate the mechanisms by which JI-CJ001 modulates HER2 signaling and autophagy in conjunction with PTX.

Main Methods:

  • Cytotoxicity assays were performed to assess cell viability.
  • Western blotting, flow cytometry, and confocal imaging were used to analyze autophagy-related pathways.
  • Mechanistic evaluations focused on HER2/mTOR signaling, STAT3, and interactions between Mcl-1 and Beclin1.
  • A gastric cancer xenograft model was utilized to evaluate in vivo anti-tumor effects.

Main Results:

  • Co-treatment with JI-CJ001 and PTX significantly suppressed gastric cancer cell growth.
  • The combination therapy reduced HER2/mTOR signaling and promoted LC3 and p62 accumulation, indicating autophagy modulation.
  • JI-CJ001 plus PTX downregulated STAT3 and disrupted the Mcl-1/Beclin1 interaction, initiating autophagy.
  • Significant anti-tumor effects were observed in the gastric cancer xenograft model.

Conclusions:

  • JI-CJ001 potentiates the therapeutic efficacy of PTX in gastric cancer by regulating HER2/mTOR signaling and autophagy.
  • The findings suggest that JI-CJ001 acts as a natural adjuvant to improve conventional chemotherapy outcomes.
  • JI-CJ001 represents a promising therapeutic strategy for overcoming chemoresistance in gastric cancer.
Keywords:
JI-CJ001JI017autophagygastric cancerpaclitaxel

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