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Receptor for Hyaluronan Mediated Motility (RHAMM)/Hyaluronan Axis in Breast Cancer Chemoresistance
Shiori Fujisawa1,2, Kiyoshi Takagi2, Mio Yamaguchi-Tanaka2,3
1Department of Breast and Endocrine Surgical Oncology, Graduate School of Medicine, Tohoku University, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Miyagi, Japan.
Cancers
|November 9, 2024
Summary
Receptor for hyaluronan-mediated motility (RHAMM) and hyaluronan (HA) are linked to breast cancer aggressiveness and recurrence. RHAMM signaling drives chemoresistance by promoting cancer stemness and epithelial-mesenchymal transition.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Receptor for hyaluronan-mediated motility (RHAMM) is a hyaluronan (HA) receptor involved in various cellular functions, including cancer.
- The role of RHAMM and HA in breast cancer chemoresistance remains largely unexplored.
- Chemoresistance presents a significant clinical challenge in breast cancer treatment.
Purpose of the Study:
- To investigate the correlation between RHAMM, HA, and breast cancer aggressiveness and recurrence.
- To explore the role of RHAMM in breast cancer chemoresistance using cell line models.
- To determine RHAMM's impact on cancer stemness and epithelial-mesenchymal transition (EMT).
Main Methods:
- Immunolocalization of RHAMM and HA in breast carcinoma tissues.
- Utilized epirubicin-sensitive (parental) and epirubicin-resistant (EPIR) breast cancer cell lines.
- Performed RHAMM knockdown experiments to assess effects on cell proliferation, migration, CD44 expression, and cadherin switching.
Main Results:
- RHAMM and HA showed a cooperative correlation with breast cancer aggressiveness and post-chemotherapy recurrence.
- RHAMM was overexpressed in chemoresistant cells, and its knockdown reduced proliferation and migration.
- RHAMM knockdown suppressed CD44 expression and promoted an epithelial phenotype by altering N-cadherin and E-cadherin levels.
Conclusions:
- Aberrant RHAMM signaling contributes to chemoresistance in breast cancer.
- RHAMM promotes cancer stemness and EMT, exacerbating chemoresistance.
- RHAMM signaling impacts both chemo-sensitive and chemo-resistant breast cancer cells, suggesting it as a therapeutic target.
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