114年-4-6-實作學生：醫學系【邱繼嶢】

參賽序號：4-6

海報主題

Apolipoprotein J Reshapes Mitochondrial Dynamic in Hormone Receptor-Positive but not in HER2-Positive Breast Cancer

系級

醫學系

指導老師及參賽學生

指導老師：孫宏羽
參賽學生：邱繼嶢

構想說明

Human epidermal growth factor receptor 2 (HER2)-positive breast cancer accounts for 20% of all breast cancer cases and is mainly treated with trastuzumab (Herceptin). However, most patients develop resistance within one year. Apolipoprotein J (ApoJ), also known as clusterin (CLU), is an extracellular chaperone involved in anti-apoptotic signaling and chemoresistance. Our previous work demonstrated that ApoJ reshapes mitochondrial dynamics and promotes malignancy in hormone receptor–positive MCF-7 breast cancer cells. Take one step forward, the present study extended the investigation to HER2-positive HCC1954 breast cancer cells. We found that trastuzumab reduced phosphorylation of the mitochondrial fission marker DRP1 and promoted mitochondrial elongation, without altering ApoJ expression. Notably, HCC1954 cells expressed a higher abundance of the ApoJ receptor LRP2 than MCF-7 cells, yet failed to uptake circulating ApoJ. Consequently, supplementation with exogenous ApoJ had no effect on mitochondrial dynamics in HCC1954 cells, indicating that ApoJ is not a key regulator in this subtype. Together, these findings reveal a unique pathological role of ApoJ in hormone receptor–positive breast cancer and underscore the importance of subtype-specific strategies for targeting mitochondrial function in breast cancer therapy.

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