Evidence map›Paper›PMID 41286438›Full record

ReviewNature reviews. Cancer2026

Targeting macropinocytosis for cancer therapy.

Daolin Tang, Jiayi Wang, Guido Kroemer, Rui Kang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Compartmental pH regulation in cancer and antitumor immunity: therapeutic opportunities and challenges.Apoptosis : an international journal on programmed cell death · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Exosomes as Emerging Nanocarriers for Targeted Cancer Therapy.International journal of nanomedicine · 2026
    Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. daolin.tang@utsouthwestern.edu.ORCID http://orcid.org/0000-0002-1903-6180
Jiayi WangDepartment of Clinical Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. jiayi.wang@sjtu.edu.cn.
Guido KroemerINSERM U1138, Équipe Labellisée - Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Université Paris Cité, Sorbonne Université, Paris, France. kroemer@orange.fr.ORCID http://orcid.org/0000-0002-9334-4405
Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA. rui.kang@utsouthwestern.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macropinocytosis is a nutrient-scavenging process that enables cells to engulf large volumes of extracellular fluid and solutes through dynamic plasma membrane ruffling. In cancer, this evolutionarily conserved process is frequently hijacked to meet the heightened metabolic demands of malignant cells, particularly under conditions of nutrient deprivation. Through macropinocytosis, tumour cells internalize diverse extracellular components - including proteins, nucleotides, lipids, ions and debris from dead cells - which are subsequently degraded in lysosomes and recycled to support biosynthesis and energy production. This process is tightly regulated by oncogenic signalling pathways and cues from the tumour microenvironment, including those associated with oncogene activation, loss of tumour suppressors and hypoxia. Beyond facilitating tumour growth and metabolic adaptation, macropinocytosis is implicated in resistance to chemotherapy, radiotherapy, targeted therapy and immunotherapy. When excessively activated, it can also lead to methuosis, a form of non-apoptotic cell death characterized by macropinosome overload. This Review outlines the molecular mechanisms and functional consequences of macropinocytosis in cancer, highlighting its dual potential as a metabolic vulnerability and a route for therapeutic delivery. Continued investigation into its regulation, context-specific roles and pharmacological modulation may uncover new opportunities for combination therapies and precision cancer treatment.

Indexed as

NeoplasmsPinocytosisAnimalsHumansSignal TransductionTumor Microenvironment

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.