# Role of the pro-inflammatory omental microenvironment in ovarian cancer progression

> **NIH CA R37** · UNIVERSITY OF TX MD ANDERSON CAN CTR · 2026 · $430,976

## Abstract

PROJECT SUMMARY/ABSTRACT
High-grade serous ovarian cancer (HGSC) metastasizes preferentially to the omentum, which is a well-
vascularized fold of peritoneal tissue covered by mesothelial cells and a major site of intra-abdominal fat
accumulation. It was reported that HGSC and stromal cell-derived pro-inflammatory cytokines downregulate
omentin (ITLN1), a novel mesothelial cell-derived adipokine to promote the invasive potential and proliferation
of cancer cells in the omental microenvironment. Omentin has been shown to suppress ovarian cancer invasive
potential and cell growth through suppressing MMP1 expression and cell traction force in cancer cells, and
inducing a local rapid metabolic coupling between ovarian cancer cells and neighboring adipocytes. Besides,
higher levels of pre-operative serum omentin in patients with HGSC were associated with longer survival times.
In addition, mice treated with omentin had marked increase in activated CD8+ T cell density compared to the
untreated control. These findings suggested that adipocytes play an important role in mediating the suppressive
effect of omentin on the malignant phenotype of ovarian cancer cells, and the immune microenvironment.
Therefore, we focus on secretory proteins that can be upregulated by omentin in mature adipocytes. A recent
proteomic study demonstrated that an anti-inflammatory protein tumor necrosis factor-inducible gene 6 protein
(TSG-6) was the top gene upregulated by omentin in adipocytes. Previous studies demonstrated that TSG-6
inhibits infiltration of immune cells during inflammation. It can also bind to specific chemokines such as CXCL12
and prevent them to bind to glycosaminoglycan (GAG)-rich tumor stroma and endothelial cell surface, suggesting
that TSG-6-mediated blockade of these cytokines to suppress tumor growth, angiogenesis, and regulatory T cell
trafficking. Based on these findings, we hypothesize that omentin normalizes the pro-inflammatory omental
microenvironment in ovarian c

## Key facts

- **NIH application ID:** 11311319
- **Project number:** 5R37CA261952-05
- **Recipient organization:** UNIVERSITY OF TX MD ANDERSON CAN CTR
- **Principal Investigator:** Chi Lam  Au Yeung
- **Activity code:** R37 (R01, R21, SBIR, etc.)
- **Funding institute:** CA
- **Fiscal year:** 2026
- **Award amount:** $430,976
- **Award type:** 5
- **Project period:** 2022-05-03T00:00:00 → 2027-04-30T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11311319

## Citation

> US National Institutes of Health, RePORTER application 11311319, Role of the pro-inflammatory omental microenvironment in ovarian cancer progression (5R37CA261952-05). Retrieved via AI Analytics 2026-06-25 from https://api.ai-analytics.org/grant/nih/11311319. Licensed CC0.

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