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MED23 in endocrinotherapy for breast cancer
Benrui Lin1, Lan Zhang2, Dinuo Li1
1Department of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P.R. China.
Abstract:
We investigated the role of the transcriptional mediator subunit 23 (MED23) in everolimus drug resistance, invasion and metastasis during breast cancer treatment and its molecular mechanism. We also evaluated the endocrinotherapy and prevention method for breast cancer. Breast cancer cell strains were established that can continuously express MED23, as well as inducible MED23-shRNA expression plasmids. The inductive agent, doxycycline (Dox), was added to the water for long-term silencing of MED23 in intratumoral cells. We conducted experiments on the role of MED23 in the regulation of invasion and metastasis of breast cancer using cell culture, western blotting, MTT proliferation experiment, fluorescent quantitative PCR and chromatin immunoprecipitation (ChIP). The silencing of MED23 significantly inhibited cellular growth and proliferation as well as soft agar cloning. Silencing of MED23 strengthened the sensitivity of the everolimus-resistant breast cancer cell strains BT474 and MCF-7/ADM cells to everolimus medication. The silencing of MED23, in combination with everolimus, inhibits the cell cycle progress of breast cancer cells. ChIP indicated that the mutual regulation of HER2 and MED23 also participates in the formation of the everolimus drug resistance mechanism. Therefore, MED23 plays an important role in everolimus drug resistance, invasion, and metastasis of breast cancer. As a potential molecular therapeutic target of breast cancer, MED23 overcomes drug resistance in clinical endocrinotherapy and controls the distal relapse and metastasis in breast cancer by the targeted silencing of MED23.
Insights
Transcriptional mediator subunit 23 (MED23) drives everolimus resistance, invasion, and metastasis in breast cancer. Silencing MED23 enhances treatment sensitivity and offers a potential therapeutic target for overcoming drug resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Breast cancer treatment faces challenges with everolimus drug resistance.
- Understanding molecular mechanisms of invasion and metastasis is crucial for effective therapy.
- Transcriptional mediator subunit 23 (MED23) role in cancer progression is under investigation.
Purpose of the Study:
- To investigate the role of MED23 in everolimus resistance, invasion, and metastasis in breast cancer.
- To elucidate the molecular mechanisms underlying MED23's function in breast cancer.
- To evaluate MED23 as a potential target for endocrinotherapy and prevention strategies.
Main Methods:
- Establishment of breast cancer cell strains with stable and inducible MED23 expression/silencing (using doxycycline).
- Cell culture, western blotting, MTT proliferation assays, quantitative PCR, and chromatin immunoprecipitation (ChIP).
- Assessment of MED23's impact on cell growth, proliferation, drug sensitivity, and cell cycle progression.
Main Results:
- MED23 silencing significantly inhibited breast cancer cell growth, proliferation, and soft agar cloning.
- Silencing MED23 resensitized everolimus-resistant cell lines (BT474, MCF-7/ADM) to everolimus.
- Combined MED23 silencing and everolimus treatment inhibited breast cancer cell cycle progression.
- ChIP analysis revealed mutual regulation between HER2 and MED23 in everolimus resistance.
Conclusions:
- MED23 is a key player in everolimus drug resistance, invasion, and metastasis in breast cancer.
- Targeted silencing of MED23 can overcome everolimus resistance in clinical endocrinotherapy.
- MED23 represents a promising molecular therapeutic target for controlling breast cancer metastasis and relapse.
