Evidence map›Paper›PMID 39092762›Full record

ReviewBiochemical Society transactions2024

Targeting endocytosis to sensitize cancer cells to programmed cell death.

Emily T Chan, Cömert Kural

Abstract readReview
In one paragraph

Review in Biochemical Society transactions, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

2 authors.

Emily T ChanInterdisciplinary Biophysics Graduate Program, The Ohio State University, Columbus, OH 43210, U.S.A.
Cömert KuralInterdisciplinary Biophysics Graduate Program, The Ohio State University, Columbus, OH 43210, U.S.A.ORCID 0000-0002-9065-6542

Funding

Utilizing Endocytic Dynamics to Obtain Comprehensive Spatiotemporal Tension Maps of Live TissuesR01GM127526 · NIGMS · OHIO STATE UNIVERSITY · PI KURAL, COMERT · 2018 to 2021
$1.8M
Molecular Biophysics predoctoral training at The Ohio State UniversityT32GM118291 · NIGMS · OHIO STATE UNIVERSITY · PI BUNDSCHUH, RALF A, KURET, JEFF · 2017 to 2021
$720k
NIGMS NIH HHS R01 GM127526NIGMS NIH HHS T32 GM118291
6 · The paper itself

Abstract

Evading programmed cell death (PCD) is a hallmark of cancer that allows tumor cells to survive and proliferate unchecked. Endocytosis, the process by which cells internalize extracellular materials, has emerged as a key regulator of cell death pathways in cancer. Many tumor types exhibit dysregulated endocytic dynamics that fuel their metabolic demands, promote resistance to cytotoxic therapies, and facilitate immune evasion. This review examines the roles of endocytosis in apoptotic resistance and immune escape mechanisms utilized by cancer cells. We highlight how inhibiting endocytosis can sensitize malignant cells to therapeutic agents and restore susceptibility to PCD. Strategies to modulate endocytosis for enhanced cancer treatment are discussed, including targeting endocytic regulatory proteins, altering membrane biophysical properties, and inhibiting Rho-associated kinases. While promising, challenges remain regarding the specificity and selectivity of endocytosis-targeting agents. Nonetheless, harnessing endocytic pathways represents an attractive approach to overcome apoptotic resistance and could yield more effective therapies by rendering cancer cells vulnerable to PCD. Understanding the interplay between endocytosis and PCD regulation is crucial for developing novel anticancer strategies that selectively induce tumor cell death.

Indexed as

ApoptosisEndocytosisNeoplasmsAnimalsAntineoplastic AgentsHumansAntineoplastic Agentscancercell deathendocytosisimmune evasionmembrane mechanics

Identifiers

PMID39092762
PMCPMC11519968

What OpenQuestion holds

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LicenceCC BY
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.