Dataset Information

The Role of FASN in bladder cancer

ABSTRACT: To dissect the mechanistic interplay between fatty acid metabolism and cigarette smoke–induced signaling in bladder cancer, we employed a proteomics analysis xenograft tumors derived from the UMUC3 with either stable FASN knockdown (KD) or control shRNA, with and without cigarette smoke. We performed global proteomics and phospho proteomics analysis to characterize the molecular alterations associated with FASN KD up on smoke exposure.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)

SUBMITTER: Antrix Jain

LAB HEAD: Putluri Nagireddy

PROVIDER: PXD068785 | Pride | 2026-06-15

REPOSITORIES: Pride

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			Action	DRS
	53510_1_EXP_1098_PDX_prof_TMT10_250ng_F01.pepXML	Pepxml
	53510_1_EXP_1098_PDX_prof_TMT10_250ng_F01.raw	Raw
	53510_1_EXP_1098_PDX_prof_TMT10_250ng_F02.pepXML	Pepxml
	53510_1_EXP_1098_PDX_prof_TMT10_250ng_F02.raw	Raw
	53510_1_EXP_1098_PDX_prof_TMT10_250ng_F03.pepXML	Pepxml

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Publications

Cigarette smoke induces FASN-dependent fatty acid metabolic rewiring to drive bladder cancer progression.

Amara Chandra Sekhar CS Piyarathna Danthasinghe Waduge Badrajee DWB Kamal Abu Hena Mostafa AHM Chan Yuen San YS Kami Reddy Karthik Reddy KR Ambati Chandra Shekar R CSR Hassan Mohammed Khurshidul MK Shriwas Pratik P Gandhi Tanmay T Jain Antrix A Gangnus Tanja T Popli Pooja P Borkar Roshan R Kang Sung Wook SW Summers Silvia L SL Putluri Vasanta V Grimm Sandra L SL Venkatesh Sharan S Song Ningxin N Seeley Erin H EH Hedlich-Dwyer Jenna J Chen Shu-Hsia SH Mahajan Nupam P NP Jain Abhinav K AK Dobrolecki Lacey Elizabeth LE Wells Gabrielle A GA Villanueva Hugo H Li Jenny J Liu Xuefeng X Bollag Roni J RJ Malovannaya Anna A Jung Sung Yun SY Lee Hyun-Sung HS Asangani Irfan A IA Terris Martha K MK Creighton Chad J CJ Ballester Leomar Y LY Karanam Balasubramanyam B Liu Suyu S Lee MinJae M Raju Rajeeva R RR Siddiqui M Minhaj MM Eberlin Livia S LS Kommagani Ramakrishna R Sreekumar Arun A Gao Jianjun J Young Nicolas L NL Hodges H Courtney HC Coarfa Cristian C Gassman Natalie R NR Lerner Seth P SP Lotan Yair Y Putluri Nagireddy N

Cancer letters 20260504

Cigarette smoke promotes bladder tumor growth by enhancing cancer cell survival and proliferation through smoke mediated carcinogens. FASN, a key enzyme in fatty acid synthesis, is dysregulated in many cancers and correlates with aggressive phenotypes. In this study, we demonstrate elevated fatty acid levels and FASN specifically in smokers with bladder cancer. Elevated FASN under smoke exposure imparted epigenetic alterations, particularly histone acetylation, impacts DNA repair and DNA-binding ...[more]

PMID: 42092682

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Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers with high mortality rate. Smoking is one of the established risk factors of ESCC. However, there is limited data on molecular alterations associated with cigarette smoke exposure in esophageal cells. Understanding the effects of cigarette smoke on esophageal squamous epithelial cells at a molecular level would lead to a better understanding of the pathobiology of ESCC which has implications for identification of early biomarkers and therapeutic targets. To investigate the effect of cigarette smoke exposure, we developed a cell line model where Het1A cells (non-neoplastic human esophageal epithelial cells) were chronically treated with cigarette smoke condensate (CSC) for 2 months, 4 months, 6 months and 8 months. We carried out comparative proteomic, phosphoproteomic and whole exome sequencing analyses on CSC treated and untreated cells. Increased cell proliferation and invasion of Het1A cells was observed after chronic exposure to cigarette smoke. Using quantitative proteomic and phosphoproteomic analyses, we identified 56 proteins and 296 phosphoproteins that showed differential expression. Bioinformatics analysis of differentially expressed proteins and phosphoproteins showed enrichment of molecules involved in DNA damage response pathway. Whole exome sequencing (WES) of CSC treated and untreated cells also revealed mutations and copy number alterations in genes associated with DNA damage response. By correlating WES, proteomic and phosphoproteomic results, we observed potential loss of function in HMGN2 and MED1 that were reported as potential tumor suppressors and are known to play important role in DNA damage response. We also observed decreased expression of HMGN2 in tissue section of ESCC. Overexpression of HMGN2 and MED1 lead to decreased proliferative and invasive ability of CSC treated cells. These findings suggest that cigarette smoke affects genes and proteins associated with DNA damage response pathways which might play a vital role in development of ESCC.