# Mechanism of Long Non-coding RNAs Action in leiomyoma

> **NIH NIH R01** · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · 2021 · $86,604

## Abstract

Uterine leiomyoma (fibroids) are benign tumors afflicting a significant number of reproductive age
women and without a known cause. Our laboratory has focused on understanding how miRNAs impact
pro-inflammatory and pro-fibrotic pathways in leiomyoma, and identified two miRNAsmiR-200c and
miR-29c which primarily target cell cycle, inflammation and extracellular matrix (ECM) component
genes respectively as key in the development of leiomyoma. Our recent findings using next generation
sequencing has demonstrated a whole host of non-coding RNAs including long non-coding RNAs
(lncRNAs) are dysregulated in fibroids. LncRNAs can act as sponge for miRNAs and therefore may be
a driver of gene dysregulation in leiomyomas. Our previous work demonstrated that tranilast, an anti-
inflammatory drug approved for the treatment of asthma in Japan and Korea, has potent effects in
fibroid cells by inhibiting cell proliferation and stimulating the expression of two key miRNAs that are
down regulated in fibroids (miR-200c and miR-29c)15, 16. These key miRNAs play a pivotal role in fibroid
pathogenesis by targeting the expression of cell cycle regulatory proteins and inflammation (miR-200c),
and composition and remodeling of the ECM (miR-29c). Furthermore, recent reports showed that H19
also can act as sponge for miR-29 and miR-200 family18-20 in various malignancies. In this project we
propose to determine if H19 can act as a sponge for miR-29/miR-200 family in fibroids and if tranilast
can decrease the expression of H19 and thereby increase the expression of miR-29 and miR-200
family. This project clearly falls within the scope of our R01 funded project exploring the interaction of
H19 with miR-29 and miR-200 family. We hypothesize that H19 sponges miR-29 and miR-200 family in
fibroids and that tranilast upregulates the expression of miR-29/miR-200 family by inhibiting the
expression of H19. This hypothesis will be tested in two Aims.
Aim 1: Determine if lncRNA H19 functions as a sponge for miR-29 and miR-200 family in fibroids, and
determine the effects of tranilast on the expression of H19 in vitro and in vivo.
Aim 2: Determine if the effect of tranilast on the expression of miR-29 and miR-200 family is mediated
 by H19.
Completion of these aims will not only advance our knowledge of the role of long non-coding RNAs in
fibroid pathogenesis and potential targeting them as a therapeutic approach but will also provide the
opportunity for our candidate Mr. Quintanilla to learn a host of new molecular and surgical techniques
and prepare him for a career in the biomedical research.

## Key facts

- **NIH application ID:** 10330338
- **Project number:** 3R01HD100529-02S1
- **Recipient organization:** LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER
- **Principal Investigator:** OMID A. KHORRAM
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $86,604
- **Award type:** 3
- **Project period:** 2020-09-08 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10330338

## Citation

> US National Institutes of Health, RePORTER application 10330338, Mechanism of Long Non-coding RNAs Action in leiomyoma (3R01HD100529-02S1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10330338. Licensed CC0.

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