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Macropinocytosis inhibition attenuates pro-fibrotic responses in lung fibroblasts and pulmonary fibrosis

ABSTRACT: We conducted a bulk RNA sequencing experiment to determine the effect of macropinocytosis inhibitor (5-(N-ethyl-N-isopropyl)-Amiloride, EIPA) in lung fibroblasts

ORGANISM(S): Homo sapiens

PROVIDER: GSE298860 | GEO | 2026/04/10

REPOSITORIES: GEO

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Macropinocytosis inhibition attenuates pro-fibrotic responses in lung fibroblasts and pulmonary fibrosis

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Cell polarity proteins promote macropinocytosis in response to metabolic stress

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Progestin receptor promotes cell macropinocytosis through CDC42 in pancreatic cancer

Project description:Endocrine receptors play an essential role in tumor metabolic reprogramming and represent a potential therapeutic approach in pancreatic ductal adenocarcinoma (PDAC). PDAC is characterized by a nutrient-deprived microenvironment, and to support their energetic needs, they can internalize extracellular proteins via macropinocytosis. In this study, we found that progesterone receptor (PGR), a steroid-responsive nuclear receptor, has a higher expression in PDAC tissues from patients and transgenic LSL-KrasG12D/+; LSL-Trp53R172H/+; PDX1-cre (KPC) mice. Moreover, PGR knockdown restrained PDAC cell survival and tumor growth both in vitro and in vivo. Genetic and pharmacological PGR inhibition resulted in dramatically macropinocytosis impairment in PDAC cells and subcutaneous tumor models, which indicates involvement of this receptor in macropinocytosis regulation. Mechanistically, PGR deficiency caused a subsequently decreased expression of CDC42, a key regulator in macropinocytosis. These data deepen our understanding of how endocrine system influences tumor progression via non-classical pathway and provide a novel therapeutic option for patients with PDAC.

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Macropinocytosis maintains CAF subtype identity under metabolic stress in pancreatic cancer [nanoString nCounter]

Project description:Pancreatic ductal adenocarcinoma (PDAC) tumors are glutamine-deficient, and both tumor cells and cancer-associated fibroblasts (CAFs) rely on this amino acid to maintain fitness and induce macropinocytosis as an adaptive response. CAFs play a critical role in sculpting the tumor microenvironment, yet how adaptations to metabolic stress impact the stromal architecture remains elusive. In this study, we find that macropinocytosis sustains the myCAF phenotype under glutamine limitation by preventing inflammatory reprogramming. Our data demonstrate that metabolic stress induces an intrinsic inflammatory CAF (iCAF) program through MEK-ERK signaling. We find that blocking macropinocytosis in vivo promotes myCAF-to-iCAF transitions, remodeling the tumor stroma. Importantly, stromal remodeling driven by macropinocytosis inhibition—including iCAF enrichment, collagen reduction, immune cell infiltration, and vascular expansion—sensitizes PDAC tumors to immunotherapy and chemotherapy. Our findings reveal that inhibiting macropinocytosis promotes an inflammatory, less fibrotic tumor microenvironment that can be leveraged to improve therapeutic responses in PDAC.

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