# Emodin as a chemopreventive agent for breast cancer - admin supp

> **NIH NIH R01** · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · 2020 · $40,361

## Abstract

PROJECT SUMMARY
It has long been suspected that tumor resection surgery may actually accelerate cancer metastasis in some
patients. Two theories for this have been proposed. The first one hypothesizes that some cancer cells are
squeezed out of the tumor into circulation during the surgical operation and travel to distant organs to form
metastasis, which grow into detectable metastasis several months later. The other hypothesizes that
subclinical micrometastases have already seeded in distant organs even before the surgery but are under
immune control, a state called metastatic dormancy, and the surgery somehow may accelerate the growth of
the micrometastases into macrometastases by breaking the dormancy. Although clinical evidences strongly
favor the second scenario, it is impractical and unethical to perform pseudo-surgery to directly test this
hypothesis in patients. A very recent elegant animal study in Dr. Robert Weinberg’s laboratory strongly
supports this scenario. Using a unique immunogenic syngeneic breast cancer mouse model, they
demonstrated that surgery wounding results in systemic inflammation, during which the inflammatory
monocytes and their resulting pro-tumor M2 macrophages (MΦs) are mobilized into circulation, leading to
accumulation of tumor-promoting MΦs in the distant organs where they facilitate the metastasis establishment
by the pre-surgery seeded of tumor cells. More interestingly, perioperative administration of meloxicam, a
nonsteroidal anti-inflammatory drug (NSAID), could significantly suppress post-surgery tumor outgrowth, which
is in line with a long time clinical observation that anti-inflammatory analgesia reduces post-surgery breast
cancer relapse. Because NSAIDs may cause immunosuppression, wound healing delay, and other severe side
effects, safer anti-inflammatory drugs are needed for this clinical application. In the past few years, our labs
discovered that a Chinese herb-derived small molecule compound, emodin, has context-dependent bi-
directional effects on MΦ activation, and can inhibit breast cancer growth and metastasis by reducing
recruitment and M2-like polarization of tumor-associated MΦs. We propose that emodin can be developed as
a safe, low-cost, and effective complementary agent to be used perioperatively to alleviate the surgery
triggered systemic inflammatory response and reduce resulting metastatic relapse of breast cancer. To test
this hypothesis, we recently developed a 4T1-derived cell line, 4T1-Luc2-RFP. Orthotopic tumors formed by
4T1-Luc2-RFP cells display much slower growth and significant resistance to metastasis. This new cell line will
present a good model with an appropriate time window to study the impact of surgery on tumor metastasis and
to develop therapeutic strategies. Two aims are proposed: 1) to test if emodin can inhibit surgical wounding
accelerated breast cancer growth and metastasis, and 2) to determine the role of macrophages in emodin’s
actions on breast cancer metastasi...

## Key facts

- **NIH application ID:** 10027034
- **Project number:** 3R01CA218578-03S1
- **Recipient organization:** UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA
- **Principal Investigator:** ELIZABETH ANGELA MURPHY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $40,361
- **Award type:** 3
- **Project period:** 2018-04-01 → 2023-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10027034

## Citation

> US National Institutes of Health, RePORTER application 10027034, Emodin as a chemopreventive agent for breast cancer - admin supp (3R01CA218578-03S1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10027034. Licensed CC0.

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