Adhesion forces between macrophages and cancer cells promote early tumor development

J Jovan Nikolic (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) J Joseph Ackermann (Laboratoire de Physique de l’Ecole normale supérieure, Ecole Normale Supérieure, Université Paris Sciences et Lettres, Centre National de la Recherche Scientifique, Sorbonne Université, Université Paris Cité) I Ines Marin (Genentech, Department of Immunology and Ophthalmology) S Sarah Taheraly (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) M Morgane Mabire (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) F François-Xavier Gobert (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) M Mathieu Maurin (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) A Apolline de Testas de Folmont (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) O Ouardia Aït-Mohamed (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) E Edison Gerena (Sorbonne Université, Centre National de la Recherche Scientifique UMR7222, Institut des Systèmes Intelligents et de Robotique) S Sophie Goyard (Institut Pasteur, Université de Paris Cité, Institut National de la Santé et de la recherche Médicale-U1224, Cell Biology of Lymphocytes) J Jérémy Mesple (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer) H Hélène Salmon (Institut Curie, Paris, France.) T Thierry Rose (Institut Pasteur, Université de Paris Cité, Institut National de la Santé et de la recherche Médicale-U1224, Cell Biology of Lymphocytes) C Christine Moussion (Genentech, South San Francisco, CA, USA.) M Martine Ben Amar (Laboratoire de Physique de l’Ecole normale supérieure, Ecole Normale Supérieure, Université Paris Sciences et Lettres, Centre National de la Recherche Scientifique, Sorbonne Université, Université Paris Cité) J Jean-François Joanny (Institut Curie Physics of Cells and Cancer/Collège de France Chair Soft Matter and Biophysics) P Philippe Benaroch (Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer)

Abstract

Biochemical mechanisms of macrophage-driven tumor promotion are well documented, but the contribution of physical forces to early tumor development remains poorly understood. Here, we combine experimental analyses with physical modeling to investigate these forces in Kras G12D p53 −/− (KP) lung tumor spheroids grown in 3D. Real-time microscopy showed that tissue-resident macrophages, but not monocytes, promote early tumor growth. Using quantitative measurements, we built a physical model that recapitulates cancer cell proliferation dynamics and macrophage–tumor interactions. KP tumor cells grown alone formed a single aggregate that contracted over time due to nutrient limitation, whereas macrophages induced the formation of multiple aggregates that grew, fused, and expanded nutrient access, thereby increasing proliferation. Similar macrophage-driven growth was observed when alveolar or bone-marrow–derived macrophages were cocultured with KP or pancreatic carcinoma cells. The model predicted a redistribution of macrophages toward the periphery of aggregates, a pattern confirmed in vitro and previously observed in vivo. It also identified adhesion forces between tumor cells and macrophages as a key driver of spheroid nucleation and growth. Among candidate integrins, CD11c was highly expressed by alveolar macrophages; CD11c blockade reduced adhesion forces, prevented macrophage-driven spheroid nucleation, and impaired tumor growth. Bone-marrow-derived macrophages required simultaneous CD11b and CD11c blockade for similar effects. Finally, CD11c inhibition in RAG-Knock Out (KO) mice reduced tumor survival probability and slowed the growth of ear-implanted tumors, indicating that CD11c-dependent interactions support tumor establishment beyond the lung. Together, these findings uncover a critical physical mechanism through which macrophages promote early tumor progression.

Article Details

Volume / Issue Vol. 123, Issue 11
Published March 17, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (18)

J

Jovan Nikolic

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

J

Joseph Ackermann

Laboratoire de Physique de l’Ecole normale supérieure, Ecole Normale Supérieure, Université Paris Sciences et Lettres, Centre National de la Recherche Scientifique, Sorbonne Université, Université Paris Cité

I

Ines Marin

Genentech, Department of Immunology and Ophthalmology

S

Sarah Taheraly

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

M

Morgane Mabire

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

F

François-Xavier Gobert

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

M

Mathieu Maurin

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

A

Apolline de Testas de Folmont

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

O

Ouardia Aït-Mohamed

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

E

Edison Gerena

Sorbonne Université, Centre National de la Recherche Scientifique UMR7222, Institut des Systèmes Intelligents et de Robotique

S

Sophie Goyard

Institut Pasteur, Université de Paris Cité, Institut National de la Santé et de la recherche Médicale-U1224, Cell Biology of Lymphocytes

J

Jérémy Mesple

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer

H

Hélène Salmon

Institut Curie, Paris, France.

T

Thierry Rose

Institut Pasteur, Université de Paris Cité, Institut National de la Santé et de la recherche Médicale-U1224, Cell Biology of Lymphocytes

C

Christine Moussion

Genentech, South San Francisco, CA, USA.

M

Martine Ben Amar

Laboratoire de Physique de l’Ecole normale supérieure, Ecole Normale Supérieure, Université Paris Sciences et Lettres, Centre National de la Recherche Scientifique, Sorbonne Université, Université Paris Cité

J

Jean-François Joanny

Institut Curie Physics of Cells and Cancer/Collège de France Chair Soft Matter and Biophysics

P

Philippe Benaroch

Institut Curie, Paris Sciences & Lettres University, Institut National de la Santé et de la recherche Médicale U932, Immunity and Cancer