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In vivo studies of the anti-tumor effects of a human prolactin antagonist, hPRL-G129R
1Oncology Research Institute, Cancer Center, Greenville Hospital System, Department of Microbiology and Molecular Medicine, Clemson University, Greenville, SC 29605, USA.
Abstract:
Previously we demonstrated that a mutated human prolactin (hPRL) with a single amino acid substitution at position 129 (hPRL-G129R) was able to inhibit human breast cancer cell proliferation via the induction of apoptosis. In this study, we report the in vivo anti-tumor effects of hPRL-G129R in nude mice bearing human breast cancer xenografts (T-47D and MCF-7). In an effort to prolong the half-life of the proteins, hPRL or hPRL-G129R were formulated with either growth factor reduced Matrigel or into slow-releasing pellets (custom made 5 mg/5 day release). Initially, nude mice inoculated (s.c.) with T-47D human breast cancer cells were treated with either hPRL or hPRL-G129R formulated with Matrigel. At the end of the 7-week study, it was found that hPRL significantly stimulated the in vivo growth of T-47D xenografts (mean tumor volume, 202 +/- 62 mm(3) as compared to 124 +/- 31 mm(3) in control mice), whereas hPRL-G129R inhibited the tumor growth (mean tumor volume, 79+/-32 mm3). The inhibitory effects of hPRL-G129R were further confirmed in a second experiment using nude mice bearing MCF-7 human breast cancer xenografts and treated with slow-releasing pellets containing hPRL-G129R. Based on these results, we believe that hPRL-G129R can be used to improve the outcome of human breast cancer treatment in the near future.
Insights
A mutated human prolactin (hPRL-G129R) effectively inhibited breast cancer xenograft growth in mice. This mutated protein offers a promising new avenue for improving human breast cancer treatment outcomes.
Area of Science:
- Endocrinology
- Oncology
- Biochemistry
Background:
- Human prolactin (hPRL) plays a role in breast cancer, but its precise effects can be complex.
- A previously identified mutated hPRL (hPRL-G129R) demonstrated in vitro inhibition of breast cancer cell proliferation by inducing apoptosis.
Purpose of the Study:
- To evaluate the in vivo anti-tumor efficacy of hPRL-G129R in mouse models of human breast cancer.
- To assess the impact of different formulations (Matrigel, slow-releasing pellets) on the protein's half-life and anti-tumor activity.
Main Methods:
- Human breast cancer xenografts (T-47D and MCF-7) were established in nude mice.
- Mice were treated with either native hPRL or mutated hPRL-G129R, formulated with Matrigel or slow-releasing pellets.
- Tumor volume was measured over a 7-week study period.
Main Results:
- Native hPRL significantly stimulated the growth of T-47D xenografts compared to controls.
- hPRL-G129R significantly inhibited the growth of both T-47D and MCF-7 xenografts.
- Formulations aimed at prolonging half-life were employed to enhance therapeutic delivery.
Conclusions:
- hPRL-G129R exhibits significant in vivo anti-tumor effects against human breast cancer xenografts.
- This mutated prolactin holds potential as a therapeutic agent for improving human breast cancer treatment.
- Further development of hPRL-G129R formulations could enhance its clinical applicability.
