Kang Ru enhances paclitaxel's efficacy against breast cancer progression

Abstract

Breast cancer and its associated drug resistance present significant clinical challenges. From a translational medicine perspective, Traditional Chinese Herbal Medicine (TCHM) offers promising integrative approach to bridge the experimental findings with clinical application, enhancing cancer treatment outcomes and mitigate drug resistance. In this study, we evaluated a TCM herbal formulation, Kang Ru (KR), comprising Artemisia argyi, Ohwia caudata, and Scoparia dulcis Linn, each traditionally and experimentally recognized for their potential therapeutic properties. We aimed to evaluate the anti-cancer effects of KR on breast cancer and its potential to enhance the efficacy of the chemotherapeutic agent paclitaxel. Using breast cancer cell lines we evaluated the effects of KR, both alone and in combination with paclitaxel on cell growth, viability, migration, and invasion. We further evaluated the potential of KR in enhancing paclitaxel to reduce tumor progression using a breast cancer xenograft model in mice. Our findings demonstrated that KR significantly inhibited cell growth and migration in breast cancer cell lines. Moreover, the combination of KR with paclitaxel demonstrated synergistic effects, effectively reducing cell viability, inducing cell apoptosis and inhibiting cell migration. In an animal model, the combination of KR and paclitaxel significantly enhanced breast cancer suppression, corroborating the in vitro findings. In conclusion, KR is a novel Chinese herbal formulation, with significant anti-cancer potential, enhancing paclitaxel's efficacy in inhibiting breast cancer progression. These findings suggest that KR could be a promising adjunctive strategy to improve breast cancer treatment and warrant further translational research to facilitate its clinical development as a complementary therapeutic option.

Keywords: Breast cancer; Kang Ru; drug efficacy; herbal formulation; paclitaxel.

Figure 1

Kang Ru (KR) reduced breast cancer cells’ viability and induced cell apoptosis dose-dependently. Breast cancer cell viability and apoptosis were assessed following treatment with KR and TAX. Both KR and TAX significantly reduced cell viability (A, B) and induced apoptosis (C, D). Results are presented as the mean ± SD from three independent experiments.

Figure 2

Combination of Kang Ru (KR) and paclitaxel (TAX) enhanced the induction of apoptosis. Breast cancer cell apoptosis was evaluated in response to combined treatment with KR and TAX. Combinations of 1000 µg/mL KR with either 10 µg/mL or 40 µg/mL TAX were used to assess the apoptotic effect. The combined treatments exhibited a significantly enhanced induction of apoptosis compared to individual treatments (A, B). Results are expressed as mean ± SD from three independent experiments.

Figure 3

Combination of Kang Ru (KR) and paclitaxel (TAX) enhanced the inhibition of breast cancer cell migration and invasion. Breast cancer cell migration and invasion were evaluated in response to the combination treatment of KR and TAX. The combination of KR and TAX significantly enhanced the inhibition of breast cancer cell migration (A, B) and invasion (C, D). Dysregulation of migration-associated markers was assessed by Western blot analysis (E, F).

Figure 4

Combination of Kang Ru (KR) and paclitaxel (TAX) enhanced the inhibition of breast cancer progression in vivo. A tumor xenograft model was established by injecting MDA-MB-231 cells into nude mice (A). After 28 days of treatment with KR and TAX, both individually and in combination, the mice were euthanized, and the tumors were resected. Tumor sizes were subsequently measured, and average sizes were calculated (B, C). Proteins extracted from the tumors were analyzed for the expression of markers associated with migration and invasion using Western blotting (D).