# Metabolic Control and Anticancer Mechanism

> **NIH NIH R01** · RBHS -CANCER INSTITUTE OF NEW JERSEY · 2021 · $341,161

## Abstract

ABSTRACT
As a central controller of cancer growth and metabolism, mTORC1 pathway is commonly mutated and activated
in human cancer, leading to uncontrolled growth. Cancer cells are ‘addicted’ to elevated mTORC1 signaling,
rendering mTORC1 a desirable cancer drug target. The highly specific mTORC1 inhibitors rapamycin analogs
(rapalogs, e.g. temsirolimus) are US FDA-approved oncology drugs. However, their clinical response has been
moderate, which is in a large part due to incomplete understanding of mTORC1 signaling mechanisms
underpinning rapamycin action. In this application, we will test the central hypothesis that nuclear mTORC1
signaling promotes aerobic glycolysis, or Warburg Effect, through a long non-coding RNA (lncRNA) NEAT1-
dependent mechanism, which is important for mTORC1-driven tumorigenesis and rapamycin response. A
successful completion of this project will provide a deeper understanding of this oncogenic pathway and
therapeutic response to its blockage.

## Key facts

- **NIH application ID:** 10198112
- **Project number:** 1R01CA260006-01
- **Recipient organization:** RBHS -CANCER INSTITUTE OF NEW JERSEY
- **Principal Investigator:** STEVEN ZHENG
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $341,161
- **Award type:** 1
- **Project period:** 2021-07-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10198112

## Citation

> US National Institutes of Health, RePORTER application 10198112, Metabolic Control and Anticancer Mechanism (1R01CA260006-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10198112. Licensed CC0.

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