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The hexosamine biosynthesis pathway in human bronchial epithelial cell transformation.

Award Number: R03CA223637
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/06/2018
PERIOD OF PERFORMANCE END DATE: 09/30/2020

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The hexosamine biosynthesis pathway in human bronchial epithelial cell transformation. - Project Description Cancer initiation and progression depend on profound alterations of cell metabolism to meet the demand for energy and biosynthesis. Elucidation of molecular mechanisms underlying this “metabolic reprogramming”, which includes increased glucose and glutamine uptake, aerobic glycolysis and altered lipid metabolism, will provide opportunities for devising novel strategies for prevention and therapy for cancers including lung cancer, a deadly disease that is a heavy public health burden. The hexosamine biosynthesis pathway (HBP) produces uridine dinucleotide phosphate-N-acetyl-glucosamine (UDP-GlcNAc) for protein glycosylation, thus couples nutrient sensing and protein quality control to metabolism and gene expression to support cell proliferation and survival. The role of HBP in lung carcinogenesis is currently unknown. Our preliminary studies suggested that L-glutamine:D-fructose-6-phosphate amidotransferase (GFAT), the rate-limiting enzyme of HBP which determines GlcNAc flux, overexpressed in lung cancer and facilitated lung cancer development and progression. The goal of this proposal is to elucidate the role of GFAT and HBP in human bronchial epithelial cell (HBEC) transformation, an early stage of lung carcinogenesis, through evaluating the communication between HBP and endoplasmic reticulum unfolded protein response, and the link of HBP to fatty acid metabolism. Two aims are designed to achieve our goal: Aim 1: To determine the mechanisms underlying GFAT induction by cigarette smoke carcinogens and the cytoprotective role of GFAT in HBECs; Aim 2: To investigate the mechanisms through which GFAT promotes HBEC transformation. We expect the data obtained from this proposal will establish a foundation for future applications further delineating the role of GFAT and HBP in lung carcinogenesis, and validate the feasibility and efficacy of targeting this pathway for lung cancer intervention.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2021 ( Subtotal = -$1,068 )
2021	2019	LOVELACE BIOMEDICAL AND ENVIRONMENTAL RESEARCH INSTITUTE, INC.	2425 RIDGECREST DR SE	ALBUQUERQUE	NM	87108	BERNALILLO	USA	Cancer Cause and Prevention Research	000	2	5/25/2021	NON-COMPETING CONTINUATION	-$1,068
														Subtotal = -$1,068

Issue Date FY: 2019 ( Subtotal = $109,000 )
2019	2019	LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE INC	2425 RIDGECREST DR SE	ALBUQUERQUE	NM	87108	BERNALILLO	USA	Cancer Cause and Prevention Research	000	2	6/19/2019	NON-COMPETING CONTINUATION	$109,000
														Subtotal = $109,000

Issue Date FY: 2018 ( Subtotal = $109,000 )
2018	2018	LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE INC	2425 RIDGECREST DR SE	ALBUQUERQUE	NM	87108	BERNALILLO	USA	Cancer Cause and Prevention Research	000	1	7/6/2018	NEW	$109,000
														Subtotal = $109,000

Grand Total All Awards = $216,932

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The hexosamine biosynthesis pathway in human bronchial epithelial cell transformation.

Award Number: R03CA223637

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/06/2018

PERIOD OF PERFORMANCE END DATE: 09/30/2020

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