Proteomics

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Neurons Release Serine to Support mRNA Translation in Pancreatic Cancer


ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) tumors have a nutrient-poor, desmoplastic, and highly innervated tumor microenvironment. Although neurons can release stimulatory factors to accelerate PDAC tumorigenesis, the metabolic contribution of peripheral axons has not been explored. We found that peripheral axons release serine (Ser) to support the growth of exogenous Ser (exSer)-dependent PDAC cells during Ser/Gly (glycine) deprivation. Ser deprivation resulted in ribosomal stalling on two of the six Ser codons, TCC and TCT, and allowed the selective translation and secretion of nerve growth factor (NGF) by PDAC cells to promote tumor innervation. Consistent with this, exSer-dependent PDAC tumors grew slower and displayed enhanced innervation in mice on a Ser/Gly-free diet. Blockade of compensatory neuronal innervation using LOXO-101, a Trk-NGF inhibitor, further decreased PDAC tumor growth. Our data indicate that axonal-cancer metabolic crosstalk is a critical adaptation to support PDAC growth in nutrient poor environments

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Pancreatic Ductal Cell, Cell Culture

DISEASE(S): Pancreatic Cancer

SUBMITTER: Miljan Kuljanin  

LAB HEAD: Joseph Mancias

PROVIDER: PXD064874 | Pride | 2025-07-07

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
JM2964_Ser_1.mzTab Mztab
JM2964_Ser_1.raw Raw
JM2965_Ser_2.mzIdentML Mzid
JM2965_Ser_2.raw Raw
JM2966_Ser_3.mzIdentML Mzid
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Publications


Pancreatic ductal adenocarcinoma (PDAC) tumors have a nutrient-poor, desmoplastic, and highly innervated tumor microenvironment. Although neurons can release stimulatory factors to accelerate PDAC tumorigenesis, the metabolic contribution of peripheral axons has not been explored. We found that peripheral axons release serine (Ser) to support the growth of exogenous Ser (exSer)-dependent PDAC cells during Ser/Gly (glycine) deprivation. Ser deprivation resulted in ribosomal stalling on two of the  ...[more]

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