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Mutant soluble Interleukin-6 receptor as a potential agent for inhibiting cell migration and inducing apoptosis in a
Maryam Sadat Mousavizadeh-Marvast1, Mina Mirian1, Fatemeh Shafiee2,3
1Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.
Objectives:
Interleukin-6 (IL-6) plays a crucial role in regulating of survival, invasion, and cell cycle of breast cancer cells. So, it appears that the suppression of IL-6 may function as a potential therapeutic agent in the context of cancer treatment. The aim of the present study is to investigate the effect of a mutated form of the soluble IL-6 receptor (mIL-6R) on the invasive ability and induction of apoptosis in MDA-MB-231 cancer cells.
Methods:
mIL-6R was expressed and purified in E. coli BL21 (DE3) bacteria and IMPACT system, respectively. The cytotoxic effects, inhibition of cell migration and apoptosis induction of mIL-6R were evaluated using MTT Assay, Scratch Assay, and Flow Cytometry assay, respectively, on the MDA-MB-231 cell line.
Results:
At a concentration of IC50 (7.41 µg.mL-1), mIL-6R inhibits cell migration and induces apoptosis, while at higher concentrations (2.IC50, 14.82 µg.mL-1), it leads to the activation of compensatory pathways and increased cell necrosis. Furthermore, disruption in the S phase of the cell cycle is observed, which may lead to DNA damage and cellular stress. mIL-6R exhibits multifaceted effects on cytotoxicity, cell migration, apoptosis, and cell cycle in a concentration-dependent manner. At IC50 (7.41 µg.mL-1), this protein primarily induced cells to enter the S phase and replicate their DNA, while at higher concentrations, such as 2.IC50 (14.82 µg.mL-1), cell cycle disruption and necrosis induction were observed.
Conclusion:
It appears that mIL-6R can act as a therapeutic candidate for breast cancer, but further investigations in animal models and clinical trials are required to determine the optimal dose and long-term effects.
Insights
A mutated form of the soluble IL-6 receptor (mIL-6R) shows potential in breast cancer therapy by inhibiting cell invasion and inducing apoptosis. Further research is needed to confirm its efficacy and optimal dosage in clinical settings.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Interleukin-6 (IL-6) is a key regulator of breast cancer cell survival, invasion, and cell cycle.
- Targeting IL-6 signaling presents a potential therapeutic strategy for cancer treatment.
Purpose of the Study:
- To investigate the effects of a mutated soluble IL-6 receptor (mIL-6R) on the invasive capabilities and apoptosis induction in MDA-MB-231 breast cancer cells.
Main Methods:
- mIL-6R was expressed and purified from E. coli.
- Cytotoxic effects, cell migration inhibition, and apoptosis induction were assessed using MTT, Scratch, and Flow Cytometry assays on MDA-MB-231 cells.
Main Results:
- At IC50 (7.41 µg/mL), mIL-6R inhibited cell migration and induced apoptosis.
- Higher concentrations (2x IC50) led to compensatory pathway activation, increased necrosis, and cell cycle disruption (S phase arrest).
- mIL-6R demonstrated concentration-dependent effects on cytotoxicity, migration, apoptosis, and cell cycle.
Conclusions:
- mIL-6R shows promise as a therapeutic candidate for breast cancer.
- Further studies in animal models and clinical trials are necessary to establish optimal dosing and long-term effects.
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